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OXFORD  MEDICAL   PUBLICATIONS 


DISEASES  OF  THE  HEART 

MACKENZIE 


OXFORD   MEDICAL   PUBLICATIONS 


DISEASES  OF  THE  HEART 


BY 


V 


JAMES  MACKENZIE,  M.D.,  M.E.C.R 


SECOND  EDITION 


OXFORD    UNIVERSITY    PRESS 

AMERICAN   BRANCH 

35  WEST  32xD  STREET,  NEW  YORK 

MCMX 


PRINTED     IN    ENGLAND 

OXFORD  :    HORACE    HART 

PRINTER    TO    THE    UNIVERSITY 


PREFACE   TO   THE   SECOND   EDITION 

The  speedy  exhaustion  of  the  first  edition  of  this  book,  and 
the  demand  for  its  translation  into  a  number  of  languages,  is  an 
evidence  of  the  interest  taken  in  the  more  recent  methods  of 
studying  diseases  of  the  heart.  It  is  extremely  gratifying  to  find 
many  investigators  entering  a  field  fidl  of  promise  of  new  and 
original  observations,  embracing  every  aspect  of  the  circulatory 
system. 

I  wish  to  point  out  that,  in  setting  forth  my  own  experiences, 
I  desire  to  keep  the  record  of  facts  apart  from  their  interpretation. 
For  this  reason  the  numerous  figures  in  the  text  represent  the 
actual  facts  as  recorded  by  the  movements  of  the  heart  and  blood- 
vessels, and  are  therefore  far  more  trustworthy  than  a  verbal 
description.  The  interpretation  of  these  tracings  represents  the 
present  state  of  my  knowledge.  These  interpretations  may  ulti- 
mately be  proved  to  be  incorrect,  but  the  recorded  movements 
will  continue  to  serve  for  other  and  more  fitting  explanations. 

A  vast  amount  of  clinical  and  experimental  work  still  remains 
to  be  done  to  explain  the  variable  changes  in  the  heart's  action 
due  to  disease,  and  my  explanations  can,  consequently,  only  be 
tentative.  Should  other  investigators  prove  these  interpretations 
wrong  by  the  discovery  of  new  facts,  I  shall  rejoice  with  them, 
for  they  will  have  shed  fresh  light,  and  will  have  reached  a  plane 
higher  than  I  have  been  able  to  attain. 

A  valuable  addition  to  the  methods  for  clinical  and  experi- 
mental observation  has  been  made  by  the  recording  of  the  electrical 
changes  caused  by  the  contraction  of  the  heart  chambers.  I  am 
indebted  to  my  friend,  Dr.  Lewis,  for  kindly  writing  a  short 
appendix  on  this  subject. 

J.  M. 

January,  1910. 


PREFACE   TO   THE   FIRST  EDITION 

In  the  following  pages  are  given  the  results  of  observations  on 
affections  of  the  heart,  made  during  an  active  practice  of  over 
a  quarter  of  a  century.  As  the  nature  of  the  heart  affection  can 
only  be  inferred  from  the  presence  of  one  or  more  symptoms,  my 
special  object  has  been  to  ascertain  the  mechanism  by  which  the 
symptoms  are  produced,  to  find  out  their  relationship  to  organic 
changes  in  the  heart,  to  ascertain  their  prognostic  significance, 
and,  finally,  to  employ  them  as  a  guide  for  treatment. 

This  line  of  observation  has  revealed  many  new  and  unexpected 
features,  and  has  necessitated  the  employment  of  special  methods 
and  the  watching  of  individual  cases  for  many  years. 

To  make  the  results  of  use  in  practice  it  has  been  found  necessary 
to  enter  into  considerable  detail,  and  it  has  been  difficult  to  make 
the  account  at  the  same  time  succinct  and  intelligible.  A  certain 
amount  of  detail  is  necessary,  yet  too  much  would  be  wearisome 
and  perhaps  confusing,  hence  controversy  has  been  avoided  and 
the  observations  have  been  given  with  the  explanation  that  seems 
most  reasonable. 

Many  methods  of  examination  that  occupy  prominent  places 
in  textbooks  have  been  briefly  dealt  with  or  even  ignored,  not 
because  I  do  not  recognize  their  usefulness  in  certain  cases,  but 
because  my  object  has  been  to  deal  with  matters  of  practical 
value  in  the  every-day  examination  of  patients.  It  may  appear 
that  an  unnecessary  amount  of  attention  has  been  devoted  to 
details,  many  of  which  can  only  be  recognized  by  special  apparatus. 
But  to  bring  conviction  proof  had  to  be  elaborated.  Many  of 
the  seemingly  trivial  signs,  such  as  the  minute  differences  in  the 
size  of  a  pulse  beat,  or  a  slight  delay  between  the  auricular  and 
ventricular  systoles,  are  really  of  vital  importance  in  revealing 


viii  PREFACE 

changes  which  have  been  proved  to  be  due  to  very  definite  affections 
of  the  heart.  In  the  same  manner  the  study  of  irregularities  is 
of  the  greatest  service,  as  their  presence  is  easily  detected  and  their 
significance  has  never  been  properly  understood.  A  close  study 
of  irregularities  throws  an  unexpected  light  upon  the  functional 
derangements  of  the  heart,  and  affords  grounds  for  an  intelligent 
diagnosis  upon  which  a  rational  treatment  and  prognosis  can  be 
based. 

The  main  purpose  of  all  my  work  has  been  to  obtain  a  guide 
for  treatment,  and  my  readers  may  be  disappointed  at  the  seeming 
barrenness  of  my  work  in  this  respect.  A  careful  search  has  been 
made  for  the  essential  principles  that  should  govern  a  rational 
treatment,  and  if  only  few  drugs  and  suggestions  are  given,  it  is 
because  the  treatment  of  cardiac  disease  at  present  in  vogue 
requires  careful  revision  in  the  light  of  the  more  accurate  diagnosis 
now  made  possible  by  means  of  the  graphic  method  of  examination. 

In  routine  practice  it  is  not  usually  necessary  to  take  graphic 
records.  If  one  is  trained  to  make  careful  and  minute  observations 
by  the  ordinary  methods,  and  to  have  these  checked  by  graphic 
records,  one  can  ultimately  acquire  the  power  of  recognizing  the 
majority  of  movements  of  the  circulation  without  graphic  records. 
In  regard  to  the  tracings  given  in  this  book,  a  selection  has  been 
made  from  an  enormous  number  of  observations,  and  are  rarely 
exceptional,  but  are  types  of  the  commoner  forms.  The  interpre- 
tation of  these  records  may  prove  to  be  faulty,  and  an  endeavour 
has  therefore  been  made  to  keep  the  actual  observation  separate 
from  the  interpretation,  so  that  if  the  latter  be  erroneous,  the 
recorded  movements  may  at  least  remain  available  for  future 
workers  in  this  field. 

It  was  originally  intended  to  give  a  more  complete  account  of 
the  morbid  anatomy  of  the  heart,  and  for  that  purpose  Professor 
Keith  has  investigated  a  great  number  of  hearts,  of  which  I  have 
kept  careful  clinical  records,  but  the  investigation,  so  far,  has 
brought  to  both  of  us  the  conviction  that  before  the  pathology  of 
the  heart  can  be  put  on  a  satisfactory  basis  a  more  thorough  and 


PREFACE  ix 

minute  examination  of  the  post-mortem  appearances  in  correlation 
with  the  clinical  symptoms  is  necessary.  The  post-mortem  aspect 
of  heart  disease  is  therefore  dealt  with  very  briefly,  and  my  obser- 
vations in  this  respect  are  intended  to  be  suggestive  rather  than 
conclusive. 

I  had  intended  to  give  the  means  of  judging  the  state  of  the 
heart  in  cases  apart  from  those  directly  due  to  affections  of  the  heart, 
as  in  fevers,  pregnancy,  surgical  diseases,  diseases  of  other  organs, 
the  administration  of  chloroform.  This  has  only  been  carried  out 
to  a  limited  extent,  because,  when  the  results  came  to  be  analysed, 
I  did  not  see  my  way  clear  in  all  cases  to  give  satisfactory  guides, 
so  that  many  observations  have  been  omitted.  I  hesitated  to 
include  my  observations  on  chloroform  administration,  because 
the  matter  is  still  very  vague.  I  feel  convinced  that  the  reason 
chloroform  is  attended  with  so  much  danger  will  never  be  solved 
until  prolonged  and  painstaking  investigation  is  made  during  its 
administration  along  the  lines  of  observation  detailed  in  this 
book  and  I  leave  my  remarks  in  this  unsatisfactory  state  in  the 
hope  that  others  may  solve  the  question. 

What  a  tool  is  to  a  workman,  so  should  a  textbook  be  to  the 
busy  practitioner.  In  cases  of  heart  affection  one  or  two  symptoms 
are  usually  most  prominent,  and  by  giving  clear  definitions  of  the 
terms  employed,  and  by  arranging  the  index  and  the  discussion  in 
the  text,  an  endeavour  has  been  made  to  facilitate  the  rapid 
inquiry  into  the  meaning  of  any  given  symptom. 

J.  M. 

17  Bentinck  Street,  London,  W. 
September,  1908. 


a  3 


CONTENTS 

PAGE 

Definition  of  Terms xviii 

CHAPTER  I  . 
General  Outline  of  the  Principles  underlying  the 

PRODUCTION    of    HeART   FAILURE 

§  1.  The  object  of  the  circulation,  and  how  it  is  attained.  §  2.  The  importance  of  the 
heart  muscle.  §  3.  The  meaning  of  heart  failure.  §  4.  Reserve  force.  §  o.  Con- 
ditions exhausting  the  reserve  force.  §  6.  The  nature  of  the  symptoms  in  heart 
failure.    §  7.  Methods  adopted  in  describing  affections  of  the  heart       ...  1 

CHAPTER  II 
Fundamental  Functions  of  the  Heart  Muscle-cells 

§8.  Myogenic  doctrine.  §9.  Stimulus  production.  §10.  Excitability.  §11.  Con- 
ductivity. §  12.  Contractility.  §  13.  Tonicity.  §  14.  Co-ordination  of  functions. 
§  15.  Characteristics  of  the  functions  of  the  heart  muscle-fibres     .  .  .  .         G 

CHAPTER  III 

Development,  Anatomy,  and  Physiology  of  the  Heart 

§  16.  The  primitive  cardiac  tube.  §  17.  The  functions  of  the  primitive  cardiac  tube. 
§  18.  The  remains  of  the  primitive  cardiac  tube  in  the  mammalian  heart.  §  19.  Func- 
tions of  the  primitive  cardiac  tissue  in  the  mammalian  heart.  §  20.  Functional 
anatomy  of  the  heart.    §21.  The  nerve-supply  of  the  heart  .  .  .  .  .11 

CHAPTER  IV 

Preliminary  Examination  of  the  Patient 

§  22.  The  patient's  appearance.  §  23.  The  patient's  sensations.  §  24.  The  patient's 
history.  §  25.  The  chief  complaints :  breathlessness,  sense  of  exhaustion,  pain, 
constriction  of  chest,  palpitation,  consciousness  of  irregular  action  of  the  heart, 
haemorrhages,  cerebral  symptoms     .........       20 

CHAPTER  V 
Respiratory  Symptoms 

§  26.  Breathlessness,  or  air  hunger.  §  27.  The  sense  of  suffocation.  §  28.  Inability  to 
stop  breathing.  §  29.  Quiet,  rapid  breathing,  free  from  distress.  §  30.  Con- 
tinuous laboured  breathing.  §  31.  Laboured  breathing  brought  on  by  exertion. 
§  32.  Attacks  of  breathlessness  (cardiac  asthma).  §  33,  Cheyne-Stokes  respiration. 
§  34.  Slow  respiration.  §  35.  Pulmonary  haemorrhage.  §  36.  Acute  suffocative 
oedema  of  the  lungs         ...........       26 


xii  CONTENTS 

CHAPTER  VI 
Reflex,  or  Protective  Phenomena 

PAGE 

§  37.  Classification  of  symptoms  in  visceral  disease.  §  38.  Insensitiveness  of  the 
viscera  to  ordinary  stimuli.  §  39.  The  mechanism  by  which  pain  and  other  reflex 
phenomena  are  produced  in  visceral  disease  (the  viscero-sensory  reflex).  §  40.  The 
purpose  of  visceral  reflexes.  §  41.  Why  pain  is  referred  to  regions  remote  from  the 
organ.  §  42.  The  relationship  of  the  heart  to  sensory  nerves.  §  43.  The  viscero- 
motor reflex.  §  44.  Vagal  sensory  reflex.  §  45.  Conditions  in  which  angina  pectoris 
is  induced.  §  4G.  Conditions  giving  rise  to  attacks  of  angina  pectoris.  §  47.  Associa- 
tion of  angina  pectoris  ^\^th  exhaustion  of  the  muscle  of  the  heart.  §  48.  Association 
of  angina  pectoris  with  impairment  of  the  function  of  contractilitj^  §  49.  Summa- 
tion of  stimuli  as  a  cause  of  angina  pectoris        .......       33 

CHAPTER  VII 
Angina  Pectoris 

§  50.  Conditions  predisposing  to  an  attack.  §  51.  Conditions  inducing  an  attack. 
§  52.  Character  and  duration  of  an  attack.  §  53.  The  symptoms  present  during  an 
attack  :  pain,  constriction  of  the  chest,  sense  of  impending  death.  §  54.  The  state 
of  the  heart  and  arteries.  §  55.  The  symptoms  present  after  an  attack.  §  56.  Estab- 
lishment of  a  tendency  to  recurrent  attacks.    §  57.  Prognosis.    §  58.  Treatment     .       45 

CHAPTER  VIII 

Heart  Affections  and  a  Hypersensitive  Nervous  System 

§  59.  Reaction  of  visceral  disease  on  the  central  nervous  system.  §  60.  Pseudo-angina 
pectoris,  a  useless  and  misleading  term.  §  61.  Exaggerated  sensory  phenomena 
with  and  without  valvular  disease.  §  62.  Exaggerated  sensory  phenomena  in 
early  cardio-sclerosis,  §  63.  Characteristics  of  the  sensory  phenomena.  §  64.  Air 
.suction.  §  65.  The  circulatory  sjmiptoms  in  the  X  disease.  §  66.  Vasomotor 
angina  pectoris.     §  67.  Prognosis.     §  68.  Treatment  ......       55 

CHAPTER  IX 
Instrumental  Methods  of  Examination 

§69,  The    sphygmograph.       §70.  Tlie    polygraph.       §71.  The     clinical     polygraph. 

§  72.  The  ink  polygraph 67 

CHAPTER  X 

The  Po.sition  and  Movements  of  the  Heart 

§  73.  The  position  of  the  heart  in  the  chest.  §  74.  The  standards  for  recognizing  the 
events  in  a  cardiac  revolution.  §  75.  Conditions  of  the  chest-wall  permitting  the 
recognition  of  certain  movements  of  the  heart.  §  76.  The  natiu-e  of  the  movements 
graphically  recorded.  §  77.  The  apex  beat.  §  78.  Interpretation  of  a  tracing  of 
an  apox  beat  due  to  the  systole  of  tlie  left  ventricle.     §  79.  The  auricular  wave. 


CONTENTS  xiii 

PAGE 

§  80.  Retraction  of  yielding  structures  in  the  neighboiuhood  of  the  heart  during 
ventricular  systole.  §  81.  Liver  movement  due  to  cardiac  aspiration.  §  82.  Epigas- 
tric pulsation.  §  83.  The  apex  beat  due  to  the  right  ventricle.  §  84.  Significance 
of  the  inverted  cardiogram.  §  85.  Alteration  of  the  apex  beat  due  to  retraction  of 
the  lung.    §  86.  The  shock  due  to  the  ventricular  systole    .....       75 

CHAPTER  XI 

Examination  of  the  Arterial  Pulse 

§  87.  Superiority  of  the  digital  examination.  §  88.  What  is  the  pulse  ?  §  89.  Inspec- 
tion of  the  arteries.  §90.  Digital  examination  of  the  arteries.  §91.  The  value  of 
a  sphygmogram.  §  92.  Definition  of  a  sphygmogram.  §  93.  Events  occurring  during 
a  cardiac  revolution  revealed  by  the  sphygmogram  :  (a)  the  systolic  period,  (6)  the 
diastolic  period.    §  94.  Features  of  the  sphygmogram  due  to  instrumental  defect    .       90 

CHAPTER  XII 
Arterial  Pressure 

§  95.  The  cause  of  arterial  pressure.  §  96.  Methods  of  measuring  the  blood-pressure. 
§  97.  Increased  blood-pressure.  §  98.  Hyperpiesis.  §  99.  Effect  on  the  heart 
of  increased  peripheral  resistance.  §  100.  Increased  arterial  pressure  and  heart 
failure.  §  101.  Treatment  of  high  arterial  pressure.  §  102.  Diminished  arterial 
pressure  .............       98 

CHAPTER  XIII 
The  Venous  Pulse 

§  103.  What  the  venous  pulse  shows.  §  104.  Inspection  of  the  jugular  pulse. 
§  105.  Methods  of  recording  the  jugular  pulse.  §  106.  The  recognition  of  the 
events  in  a  jugular  pulse.  §  107.  Description  of  the  events  in  a  cardiac  cycle. 
§  108.  The  causes  of  variation  of  pressure  in  the  auricle  and  in  the  jugular 
vein.  §  109.  Standards  for  interpreting  a  jugular  tracing.  §  110.  The  carotid 
wave.  §  111.  The  notch  on  the  ventricular  wave.  §  112.  The  diastolic  wave. 
§  113.  Changes  due  to  variation  in  the  rate  of  the  heart.  §  114.  Method  of  analys- 
ing a  tracing.  §  115.  The  ventricular  form  of  the  venous  pulse.  §  116.  Conditions 
giving  rise  to  a  venous  pulse    ..........     105 

CHAPTER  XIV 

Enlargement  and  Pulsation  of  the  Liver 

§  117.  Reflex  or  protective  symptoms.  §  118.  Signs  of  enlargement  of  the  liver. 
§  119.  Pulsation  of  the  liver.  §  120.  Conditions  producing  enlargement  and 
pulsation  of  the  liver.  §  121.  Jaundice.  §  122.  Differential  diagnosis.  §  123. 
Prognosis.     §  124.  Treatment    ..........     122 

CHAPTER  XV 

Increased  Frequency  of  the  Heart's  Action 

§  125.  The  normal  rate.  §  126.  Classification.  §  127.  Cases  which  respond  to  a  call 
upon  the  heart's  energy  by  increased  frequency.    §  128.  Cases  in  which  the  heart's 


xiv  CONTENTS 

PAGE 

rate  is  continuously  increased.  §  129.  Cases  in  which  the  increased  frequency  of 
the  heart  occurs  in  irregular  paroxysmal  attacks  (palpitation).  §  130.  The  cause 
of  increased  frequency  of  the  heart's  action.    §  131.  Prognosis     ....     129 

CHAPTER  XVI 

Diminished  Frequency  of  the  Heart's  Action 

§  132.  Definition  of  the  term  '  bradycardia  '.    §  133.  Normal  bradycardia    .  .         .     138 

CHAPTER  XVII 
The  Irregular  Action  of  the  Heart 

§  134.  Places  where  the  heart's  contraction  may  start.  §  135.  Classification  of  irregu- 
larities   ..............     140 

CHAPTER  XVIII 

Sinus  Irregularities 

§  136.  Character  of  the  irregularity.  §  137.  Etiology.  §  138.  Symptoms.  §  139.  Asso- 
ciated symptoms.    §  140.  Prognosis  .........     143 

CHAPTER  XIX 
The  Extra-systole 

§  141.  Definition  of  the  term  '  extra-systole '.  §  142.  Character  of  the  irregularity. 
§  143.  Etiology.       §  144.  Ventricular     extra-systole.  §  145.  Auricular     extra- 

systole.  §  146.  Nodal  extra-systole.  §  147.  Condition  of  the  a. -v.  bundle  in 
cases  showing  extra-systoles.  §  148.  The  dropping  out  of  the  beat  after  the  extra- 
systole.  §  149.  Reasons  for  attributing  the  origin  of  extra-systoles  to  affections  of 
the  remains  of  the  primitive  cardiac  tube.  §  150.  Conditions  inducing  extra-systoles. 
§  151.  Sensations  produced  by  extra-systoles.    §  152.  Prognosis.    §  153.  Treatment     148 

CHAPTER  XX 

The  Nodal  Rhythm  (Continuous  Irregularity  of  the 
Heart — Paroxysmal  Tachycardia) 

§  154.  Meaning  of  the  term  '  nodal  rhythm  '.  §  155.  Etiology.  §  156.  Manner  in  which 
the  nodal  rhythm  leads  to  heart  failure.  §  157.  Classification.  §  158.  Cases  in 
which  the  rate  is  not  markedly  increased.  Symptoms.  Prognosis.  Treatment. 
§  159.  Cases  in  which  the  rate  is  greatly  increased.  Symptoms.  Prognosis.  Treat- 
ment. §  160.  Cases  in  which  the  nodal  rhythm  is  transient  and  recurrent  (par- 
oxysmal tachycardia).    Symptoms.    Piognosis.    Treatment .         .  .  .  .166 

CHAPTER  XXI 

Affections  of  the  Conducting  Functions  of  the  Primitive  Cardiac 
Tissue  (Heart-Block,  Adams-Stokes  Disease,  Ventricular  Rhythm) 

§  161.  Definition.  §  162.  Methods  of  recognizing  depression  of  conductivity.  §  163. 
Intersystolic  period  (the  a-c  interval).  §  164.  Depression  of  conductivity  without 
arrhythmia.     §  165.  Influence  of  rest  upon  conductivity.     §  166.  Arrhythmia  due 


CONTENTS  XV 

PAGE 

to  depression  of  conductivity.  §  167.  Missed  beats  due  to  depression  of  conductivity. 
§  168.  Independent  ventricular  rhythm  due  to  heart-block.  §  169.  Effect  of  the 
auricular  contraction  on  the  radial  pulse.  §  170.  Etiology.  §  171.  Significance 
of  the  milder  forms  of  depression  of  conductivity.  §  172.  Symptoms.  §  173.  Prog- 
nosis.    §  174.  Treatment  ...........     175 

CHAPTER  XXII 
Exhaustion  of  Contractility 

§  175.  Necessity  for  recognizing  exhaustion  of  contractility.  §  176.  The  function  of 
contractility.  §  177.  Conditions  inducing  exhaustion  of  contractility.  §  178.  Symp- 
toms :  (a)  reflex,  (6)  changes  in  the  heart's  action.  §  179.  The  pulsus  alternans. 
§  180.  Prognosis.     §  181.  Treatment 191 

CHAPTER  XXIII 
Dilatation  of  the  Heart  (Failure  of  Tonicity) 

§  182.  The  cause  of  dilatation  of  the  heart.  §  183.  The  function  of  tonicity.  §  184.  The 
symptoms  of  depression  of  tonicity.  §  185.  Dilatation  of  the  heart.  §  186.  The 
cause  of  functional  murmurs.  §  187.  The  consequences  of  dilatation  of  the  heart, 
and  how  they  are  brought  about.  §  188.  Dropsy.  §  189.  Enlargement  of  the  liver. 
§  190.  Oedema  of  the  lungs.  §  191.  Urinary  symptoms.  §  192.  Prognosis. 
§  193.  Treatment  201 

CHAPTER  XXIV 

Acute  Febrile  Affections  of  the  Heart 

§  194.  Manner  in  which  the  heart  is  affected  in  fever.  §  195.  The  febrile  heart. 
§  196.  Acute  febrile  affections  of  the  heart.  §  197.  Symptoms  in  myocarditis : 
changes  in  rate,  changes  in  rhythm  due  to  depressed  conductivity  of  the  a. -v.  bundle, 
depressed  contractility,  extra-systole,  nodal  rhythm,  depressed  tonicity  (dilatation 
of  the  heart).  §  198.  Symptoms  in  endocarditis.  §  199.  Symptoms  in  pericarditis. 
§  200.  The  heart  in  rheumatic  fever  :  pathological  changes,  symptoms.  §  201.  The 
heart  in  pneumonia.  §  202.  The  heart  in  diphtheria.  §  203.  The  heart  in  septic 
infections.    §204.  Treatment 214 

CHAPTER  XXV 
Valvular  Defects 

§  205.  The  manner  of  heart  failure  with  valvular  defects.  Mitral  stenosis  :  §  206.  Con- 
ditions inducing  heart  failure  in  mitral  stenosis.  §  207.  Murmm-s  present  in  mitral 
stenosis  (presystolic,  diastolic,  disappearance  of  the  presystolic  murmur,  presy- 
stolic murmm-  of  ventricular  origin,  systolic  murmur  due  to  mitral  stenosis).  §  208. 
Progress  and  symptoms  in  mitral  stenosis.  §  209.  Occasional  symptoms  :  paroxys- 
mal tachycardia,  haemoptysis,  cerebral  embolism,  angina  pectoris.  Mitral  regurgita- 
tion :  §210.  Murmurs  due  to  mitral  regurgitation.  §211.  Conditions  inducing 
heart  failure  in  mitral  regurgitation  .........     228 


xvi  CONTENTS 

CHAPTER  XXVI 

Valvular  Defects  (continued) 

PAGE 

§  212.  Tricuspid  incompetence.  §  213.  Tricuspid  stenosis.  §  214.  Disease  of  the  aortic 
valves.  Etiology.  §  215.  Aortic  stenosis.  §  216.  Aortic  incompetence.  §  217. 
Prognosis  in  valvular  affections.     §  218.  Treatment     ......     237 

CHAPTER  XXVII 

Cardio-Sclerosis  (Arterial  Degeneration.    The  Senile  Heart) 

§219.  Conditions  producing  cardio-sclerosis.  §220.  Conditions  inducing  degenerative 
changes  in  the  arterial  system,  §  221.  Obliteration  of  the  capillaries.  §  222.  Symp- 
toms of  cardio-sclerosis.     §  223.  Prognosis.     §  224.  Treatment.     §  225.  Aneurysm    243 

CHAPTER  XXVIII 
Adhesive  Mediastino-Pericarditis 

§  226.  Etiology.    §  227.  Symptoms.    §  228.  Prognosis  and  treatment  ....     253 

CHAPTER  XXIX 

Congenital  Affections  of  the  Heart 

§229.  Etiology.     §230.  Symptoms.     §231.  Prognosis.     §232.  Treatment  .         .         .256 

CHAPTER  XXX 
Heart  Disease  and  Pregnancy 

§  233.  Importance  of  the  subject.     §  234.  Standards  for  guidance.    §  235.  Management 

of  the  labour 258 

CHAPTER  XXXI 

Chloroform  in  Heart  Affections 

§  236.  Conditions  contra-indicating  its  use  :  respiratory  embarrassment,  cardio-sclerosis, 

status  lymphaticus.    §  237.  Estimation  of  the  fitness  of  the  patient       .  .  .     261 

CHAPTER  XXXII 

Prognosis 

§  238.  Responsibility  of  the  medical  profession.    §  239.  Basis  for  prognosis   .         .         .     264 

CHAPTER  XXXIII 
Treatment 

§240.  The  essential  principle  in  treatment.  §241.  Rest.  §242.  Sleep.  §243.  Bodily 
comfort.  §  244.  Diet.  §  245.  Condition  of  the  bowels.  §  246.  The  mental  factor. 
§247.  Drugs.     §248.  Oxygen 268 


CONTENTS  xvii 

CHAPTER  XXXIV 

Treatment  (continued) 

PAGE 

§  249.  The  action  of  digitalis  on  the  human  heart.  §  250.  Action  on  dilatation  of  the 
heart.  §  251.  Action  on  rate  and  on  the  nodal  rhythm.  §  252.  Action  on  conduc- 
tivity (heart-block).  §  253.  Action  on  contractility.  §  254.  Action  on  blood- 
pressure.  §  255.  Digitalis  in  practice.  §  256.  Other  drugs  of  the  digitalis  group 
(strophanthus,  squills,  helleborein)       .......        281 

CHAPTER  XXXV 

Treatment  (continued) 
§  257.  Venesection.    §  258.  Exercises.    §  259.  Massage.    §  260.  Special  movements  and 
exercises.     §261.  Baths.     §262.  Spa  treatment.     §263.  Nauheim  baths.     §264. 
Cause  of  efficacy  of  the  spa  treatment     .......        293 

APPENDIX  I 
The  Pulse  in  Angina  Pectoris  .......      302 

APPENDIX  II 

The  Nodal  Rhythm    .........      309 

APPENDIX  III 
Paroxysmal  Tachycardia  of  Auricular  Origin  ,         .         .334 

APPENDIX  IV 
Nodal  Bradycardia   .........      337 

APPENDIX  V 
Irregularities  in  Cardio-Sclerosis    ......      350 

APPENDIX  VI 

The  Effects  of  Digitalis  on  the  Human  Heart        .         .         .356 

APPENDIX  VII 

The  Electro-cardiogram    ........      370 

BIBLIOGRAPHY 377 

INDEX 395 


DEFINITION   OF  TERMS 

Although  I  have  endeavoured  in  the  text  to  explain  clearly  what  I  mean  by  any  term, 
yet  many  terms  -will  be  employed  before  the  reader  reaches  the  places  where  they  are 
explained.  For  that  reason  I  give  here  a  brief  description  of  the  more  important  terms  that 
have  been  lately  introduced  or  are  not  found  in  current  literature,  or  which  I  have  employed 
to  describe  conditions  that  have  not  been  hitherto  recognized. 

a.-c.  interval  is  the  time  between  the  beginning  of  the  auricular  and  carotid  waves  in  tracings 
of  the  jugular  pulse.     (Also  intersystolic  period  described  in  §  163.) 

Arterial  degeneration  is  the  term  used  to  cover  all  forms  of  arterial  disease.  As  I  deal 
with  arterial  disease  only  so  far  as  it  embarrasses  the  work  of  the  heart,  I  use  this  to  avoid 
the  more  specific  terms  concerning  which  there  is  still  so  much  difference  of  opinion. 

Auricular  venous  pulse  is  the  form  of  jugular  pulsation  where  the  wave  due  to  the  auricle 
is  found  preceding  the  ventricular  contraction  in  contradistinction  to  the  ventricular 
venous  pulse  (q.v.).     Sometimes  called  also  the  normal  or  negative  venous  pulse. 

Auriculo-ventricular  node  (a.-v.  node,  Knoten  of  Tawara)  is  the  enlargement  of  the  remains 
of  the  primitive  cardiac  tissue  found  in  the  wall  of  the  right  auricle,  from  which  the  a.-v. 
bimdle  arises  (Fig.  2). 

Auriculo-ventricular  bundle  (a.-v.  bundle,  Gaskell's  bridge,  Kent's  or  His's  bundle).  The 
remains  of  the  primitive  cardiac  tissue  which  passes  from  the  a.-v.  node  to  the  right  and 
left  ventricles. 

Card  io-sclero  sis.  Fibrous  changes  affecting  the  endocardium  and  myocardium  are  found 
in  the  majority  of  cases  in  two  groups  of  people,  those  with  a  history  of  an  acute  febrile 
affection — most  commonly  rheumatic  fever — and  those  with  evidences  of  arterial  degenera- 
tion. The  symptoms  resulting  from  both  conditions  have  a  great  similarity,  but  there 
are  circumstances,  such  as  age  and  response  to  treatment,  that  sharply  separate  them  ; 
the  term  cardio-sclerosis,  unless  qualified,  will  always  refer  to  the  group  with  arterial 
degeneration.  Fatty  changes  are  frequently  present  in  cardio-sclerosis,  but  they  cannot 
be  distinguished  by  clinical  methods. 

Conductivity  is  the  term  used  by  Gaskell  to  describe  that  function  of  the  fibres  of  the  heart 
muscle  which  conveys  the  stimulus  from  fibre  to  fibre.  It  is  usually  studied  by  observing 
the  time  between  the  systole  of  the  auricles  and  ventricles. 

Contractility  is  Gaskell's  term  for  the  power  of  contracting  possessed  by  the  muscle. 

Extra-systole  is  the  premature  contraction  of  the  auricle  (auricular  extra- systole)  or  of  the 
ventricle  (ventricular  extra-systole),  or  both  chambers  together  (nodal  extra-systole), 
while  the  fundamental  or  sinus  rhythm  is  maintained.  Usually  the  extra-systole  is 
followed  by  a  long  pause  (compensatory  pause).  Karely  the  premature  contraction 
occurs  between  two  normal  beats  (interpolated  extra-systole). 


DEFINITION  OF  TERMS  xix 

Heart-block  is  the  term  used  by  Gaskell  to  signify  the  stoppage  or  blocking  of  the  stimulus 
for  contraction  in  its  passage  from  the  auricles  to  the  ventricles. 

Hyperalgesia.  An  abnormal  sensitiveness  to  pain,  shown  by  a  painful  response  to  such 
stimulation  as  would  not  normally  produce  pain,  e.  g.  lightly  pressing  the  skin  (cutaneous 
hyperalgesia)  or  muscles  (muscular  hyperalgesia)  between  the  thumb  and  forefinger. 

Myogenic  theory.  The  view  that  the  heart  muscle-fibres  possess  in  themselves  the  power 
of  originating  and  conveying  the  stimulus  for  the  contraction  of  the  heart,  as  opposed 
to  the  neurogenic  theory,  where  it  is  held  that  the  heart  acts  only  in  response  to  nerve 
stimulation. 

Nodal  Bradycardia  is  the  term  used  for  that  condition  of  infrequent  action  of  the  heart 
where  there  is  no  evidence  of  the  auricular  systole  between  the  ventricular  beats  and 
where  the  venous  and  liver  pulses  are  of  the  ventricular  form  (see  also  Nodal  Ehythm). 

Nodal  rhythm.  In  the  majority  of  cases  of  continuous  irregularity  and  paroxysmal  tachy- 
cardia it  is  found  that  the  ventricular  contraction  precedes  or  is  sjTichronous  with  the 
auricular  contraction,  and  hence  it  is  inferred  that  the  heart's  contraction  in  these  cases 
must  originate  from  a  point  that  could  affect  both  auricle  and  ventricle  at  or  about  the 
same  time.  It  is  suggested  that  this  point  may  be  in  the  a.-v.  node  or  its  neighbourhood, 
and  as  it  is  important  to  recognize  the  abnormal  rhythm  it  is  provisionally  distinguished 
by  the  term  '  nodal  rhythm  '.* 

Palpitation  is  used  in  a  twofold  sense,  to  describe  (a)  attacks  of  increased  frequency  of  the 
heart's  action,  (6)  the  sensation  by  which  a  patient  is  conscious  of  the  excited  and  usually 
increased  frequent  action  of  the  heart. 

Paroxysmal  tachycardia  is  applied  to  a  sudden  increase  in  the  heart's  rate,  usually 
followed  by  an  equally  sudden  reversion  to  the  normal.  It  is  due  to  the  starting  of  the 
heart's  contraction  at  some  part  other  than  the  normal.  The  most  common  form  is  really 
a  transient  nodal  rhythm.  There  is  also  a  rarer  form,  where  the  stimulus  arises  in  the 
auricle.  I  therefore  restrict  the  term  to  the  increased  frequency  of  the  heart's  action 
due  to  the  temporary  inception  of  an  abnormal  rh3rthm. 

Primitive  cardiac  tissue  is  the  term  applied  to  the  tissue  in  the  mammaUan  heart  which 
represents  the  cardiac  tube  of  the  more  primitive  vertebrates.  It  is  shown  in  Fig.  2, 
and  consists  of  the  s.-a.  and  a.-v.  nodes  and  a.-v.  bundle.  This  view  of  the  origin  of 
these  structures  is  inferred  from  the  consideration  of  certain  embryological,  physiological, 
and  clinical  characteristics,  but  has  not  yet  been  fully  estabUshed  by  embryologists. 

Pulsus  alternans  means  that  form  of  abnormal  rhjrthm  where  the  radial  pulse  is  perfectly 
regular  but  where  there  is  an  alternation  in  the  size  of  the  beats,  and  is  an  evidence  of 
the  failure  of  the  function  of  contractility. 

Pulsus  bigeminus  is  applied  to  that  form  of  pulse  irregularity  where  every  second  beat  is 
an  extra-systole,  and  is  usually  smaller  than  the  preceding  normal  beat.  The  smaller 
beat  is  invariably  followed  by  a  pause  longer  than  the  pause  preceding  it. 

Sino-auricular  node  (s.-a.  node).  The  term  given  by  Keith  and  Flack  to  a  small  bundle 
of  tissue  representing  the  remains  of  the  primitive  cardiac  tube  (portion  of  the  sinus 
venosus)  near  the  mouth  of  the  superior  vena  cava  (1,  Fig.  2). 

Tonicity  is  the  term  applied  to  that  function  of  the  heart  muscle  which  keeps  the  heart  during 
diastole  in  a  state  of  slight  contraction.  Depression  of  this  function  results  in  dilatation 
of  the  heart  and  of  the  auriculo-ventricular  orifices. 

*  Resent  elestro-cardiographic  observatioas  by  Lewis  leads  him  to  conclude  that  the  dis- 
appearance of  the  evidence  of  the  auricular  contraction  in  cases"  of  nodal  rhythm  is  often  due  to 
the  auricle  passing  into  fibrillation. 


XX 


DEFINITION  OF  TERMS 


Ventricular  rhythm.  This  term  is  applied  to  the  ventricular  contractions  in  cases  of  complete 
heart-block.  As  this  occurs  when  a  lesion  severs  the  a. -v.  bundle,  it  is  assumed  that  the 
remaining  fibres  of  the  a. -v.  bxindle  in  the  ventricles  start  the  ventricular  contractions,— 
the  rate  being  very  slow,  rarely  above  thirty-two  beats  per  minute.  (In  some  of  my 
earUer  witings  I  employed  this  term  to  describe  the  condition  given  under  nodal 
rhythm.) 

Ventricular  venous  pulse  is  that  form  of  jugular  pulsation  in  which  the  auricular  wave 
disappears  or  coincides  with  the  period  of  ventricular  systole,  there  being  no  sign  of  the 
auricular  wave  at  the  normal  period  of  the  cardiac  cycle.  Sometimes  called  the  positive 
or  pathological  venous  pulse. 

Viscero-motor  reflex.  The  term  used  to  describe  the  contraction  of  muscles  of  the  external 
body- wall  in  response  to  a  stimulation  from  a  diseased  viscus. 

Viscero-sensory  reflex.  The  sensory  symptoms  (pain  and  hyperalgesia)  evoked  by  the 
stimulation  from  a  diseased  viscus  of  a  sensory  nerve  in  its  passage  from  its  peripheral 
distribution  in  the  external  body-wall  to  the  brain. 


DISEASES   OF   THE   HEART 

CHAPTER  I 

General  Outline  of  the  Principles  underlying  the  production 

OF  Heart  Failure 

§  I.  The  object  of  the  circulation,  and  how  it  is  attained. 

2.  The  importance  of  the  heart  muscle. 

3.  The  meaning  of  heart  failure. 

4.  Reserve  force. 

5.  Conditions  exhausting  the  reserve  force. 

6.  The  natiire  of  the  symptoms  in  heart  failure. 

7.  Methods  adopted  in  describing  affections  of  the  heart. 

As  the  study  of  the  condition  of  the  heart  is  approached  in  this  book 
from  a  standpoint  somewhat  different  from  that  usually  taken  in  textbooks 
on  diseases  of  the  heart,  I  propose  to  give  here  a  brief  description  of  the 
principles  underlying  this  method  of  study,  in  order  that  the  reader  may 
the  more  readily  appreciate  the  nature  and  symptoms  of  heart  failure. 

§  I.  The  object  of  the  circulation,  and  how  it  is  attained. — The 
object  of  the  circulation  is  the  supply  of  a  constant  stream  of  material  capable 
of  nourishing  the  tissues,  and  of  replacing  the  loss  of  energy  sustained  by 
them,  and  the  removal  of  such  waste  products  as  are  capable  of  entering 
the  circulatory  channels.  In  order  to  facihtate  the  exchange  of  products 
between  the  blood  and  the  tissues,  a  certain  degree  of  slowing  of  the  flow 
takes  place  as  the  blood  passes  through  the  capillaries.  As  a  continuous 
pressure  is  required  to  force  the  blood  onwards,  the  intermittent  pressure 
conveyed  to  the  blood-stream  by  the  heart  is  converted  by  the  resihent 
nature  of  the  arterial  walls  into  a  constant  pressure  at  the  periphery  of  the 
arterial  system.  The  maintenance  of  the  arterial  pressure  is  the  outcome 
of  the  force  exerted  by  the  left  ventricle,  and  of  the  resistance  of  the  smaller 
a,rteries  and  capillaries.  The  full  force  of  the  ventricular  contraction  is 
not  spent  on  the  blood-current  merely  during  the  period  of  its  systole.  In 
throwing  the  bloodj^into  the  arterial  system,  it  does  so  with  such  force  that 
it  distends  to  a  sUght  extent  the  larger  arteries.  The  elastic  coats  of  the 
arteries,  as  soon  as  the  ventricular  systole  is  over,  compress  the  column  of 
blood  within  them,  and  in  this  manner  maintain  a  degree  of  arterial  pressure 
during  the  period  that  the  ventricle  is  not  acting.     The  ventricular^force 


MACKENZIE 


2  DISEASES  OF  THE  HEART 

is  thus  stored  up  by  the  distension  of  the  elastic  coats  of  the  arteries,  and 
liberated  during  the  ventricular  diastole. 

The  principles  underlying  the  mode  of  action  of  the  left  ventricle  and 
the  systemic  circulation  apply  equally  to  the  right  ventricle  and  the  pul- 
monary circulation. 

§  2.  The  importance  of  the  heart  muscle. — The  heart  muscle  supphes 
the  force  which  maintains  the  circulation.  In  the  normal  condition,  the 
mechanism  of  the  circulation  is  so  adjusted  that  all  parts  combine  to  facihtate 
the  work  of  the  heart  and  to  attain  the  object  of  the  circulation.  Any  dis- 
turbance of  that  adjustment  must  at  once  entail  more  work  upon  the  heart 
muscle,  inasmuch  as  a  departure  from  the  normal  means  the  embarrassment  of 
the  heart  in  maintaining  the  normal  arterial  pressure.  So  long  as  the  heart 
can  overcome  the  impediment,  and  maintain  the  circulation  in  a  normal 
manner,  no  symptoms  are  evoked,  but  if  the  heart  is  no  longer  able  to  carry 
on  the  circulation  efficiently,  then  certain  phenomena  at  once  arise,  and 
these  phenomena  we  call  '  symptoms  of  heart  failure  '. 

§  3.  The  meaning  of  heart  failure. — From  this  consideration  it  will 
be  reahzed  that  heart  failure  is  simply  inabihty  of  the  heart  muscle  to 
maintain  the  circulation,  and  that  this  failure  of  the  heart  muscle  is  due 
to  a  disturbance  of  the  normal  adjustment  of  the  various  factors  concerned 
in  the  circulation.  This  disturbance  may  arise  in  a  great  many  ways,  but 
the  end  result  is  the  same — embarrassment  of  the  heart  muscle  and  its  final 
exhaustion.  The  heart  muscle,  therefore,  is  of  such  prime  importance  in 
what  we  call  heart  failure,  that  a  close  and  intimate  study  of  its  properties 
is  essential.  This  will  be  dealt  with  later  in  some  detail ;  here  I  want  to 
call  attention  to  a  feature  of  the  heart  muscle  which  is  the  essential  factor 
in  the  consideration  of  every  form  of  heart  failure,  namely,  the  reserve 
force. 

§  4.  Reserve  force. — If  the  part  played  by  the  heart  muscle  in  the 
maintenance  of  the  circulation  and  the  nature  of  the  symptoms  in  heart 
failure  be  considered,  it  wiU  be  found  that  the  explanation  of  heart  failure 
can  be  summed  up  in  the  general  statement  that  heart  failure  is  due  to  the 
exhaustion  of  the  reserve  force  of  the  heart  muscle  as  a  whole,  or  of  one  or 
more  of  its  functions.  This  statement  may  seem  so  self-evident  as  scarcely 
to  need  amplification,  but,  as  a  matter  of  fact,  this,  the  essential  principle 
on  which  diagnosis,  prognosis,  and  treatment  should  be  based,  is  often 
practically  ignored.  I  shall  make  no  apology  for  the  continuous  reiteration 
of  this  apparent  truism,  for  the  simple  reason  that  in  the  study  of  aU  cases 
of  heart  failure  the  condition  of  the  reserve  force  will  be  found  to  be  the 
ultimate  question. 


GENERAL  OUTLINE  OF  HEART  FAILURE  3 

Although  we  recognize  what  reserve  force  is,  it  is  not  very  easy  to  define 
it  in  words.  Physiologists  do  not  seem  to  have  given  it  that  study  its  impor- 
tance demands.  Although  difficult  to  define,  its  existence  is  proved  in  every 
movement  of  the  body,  and  in  every  effort  which  is  made,  as  it  is  by  the 
possession  of  this  quality  that  we  are  able  Avith  ease  to  undertake  all  forms 
of  effort.  The  estimation  of  the  amount  of  reserve  present  is  the  best  test 
of  the  heart's  condition.  It  is  the  'premature  exhaustion  of  this  reserve  ivhich 
constitutes  heart  failure,  and  it  is  the  heart's  power  to  regain  this  reserve 
force  on  which  recovery  from  heart  failure  depends. 

§  5.  Conditions  exhausting  the  reserve  force. — I  have  already  re- 
marked that,  in  the  normal  condition,  the  adjustment  of  all  parts  concerned 
in  carrying  on  the  circulation  is  essential  to  efficiency.  Any  disturbance 
of  the  adjustment  at  once  calls  for  an  increased  effort.  Such  calls  are  made 
first  on  the  reserve  force  and,  if  persisted  in,  lead  sooner  or  later  to  its 
exhaustion.  These  disturbances  of  the  adjustment  are  extraordinarily 
varied  in  character,  and  may  arise  from  any  one  of  the  factors  on  which 
the  normal  heart's  action  depends.  It  will  be  from  this  standpoint  that 
the  diseases  of  the  heart  will  be  studied,  inasmuch  as  it  is  only  by  looking 
at  the  matter  in  this  hght  that  a  proper  perspective  is  obtained  in  regard 
to  the  significance  of  any  abnormahty.  Thus,  irregular  action  of  the  heart 
will  be  described  from  the  point  of  view  of  its  effect  upon  the  efficient 
performance  of  the  heart,  as  well  as  the  condition  producing  it.  Valvular 
defects  will  be  studied  not  as  a  specific  affection  to  be  considered  in  them- 
selves, but  rather  as  a  source  of  embarrassment  to  the  heart  muscle  in  its 
work.  In  the  same  manner,  arterial  degeneration  and  high  blood-pressure 
wiU  be  considered  as  conditions  that  upset  the  normal  adjustment  of  the 
factors  that  carry  on  the  circulation.  Inherent  defects  of  the  muscular 
wall  itself  wiU  also  be  viewed  in  their  bearing  on  the  heart's  efficiency.  The 
relative  efficiency  of  independent  functions  of  the  muscle-fibres  will  be  kept 
constantly  in  view,  inasmuch  as  organic  lesions  act  deleteriously  through 
disturbing  the  normal  harmony  of  these  functions.  Depression  of  the  in- 
dividual functions  may  arise  without  any  gross  organic  lesions,  and  lead  to 
serious  embarrassment  of  the  circulation.  "While  I  am  far  from  compre- 
hending the  full  effect  of  functional  depression,  for  the  study  of  pure  func- 
tional pathology  is  in  its  infancy,  yet  I  hope  the  facts  I  detail  may  help 
forward  a  line  of  observation  that  promises  much  for  future  investigation. 

§  6.  The  nature  of  the  symptoms  in  heart  failure. — Briefly  put, 
the  symptoms  are  produced  by  the  exhaustion  of  the  reserve  force.  The 
first  sign  is  invariably  a  subjective  one,  although  it  may  for  a  time  pass 
unnoticed.     The  patient's  attention  is  first  directed  to  his  condition  by  some 

B  2 


4  DISEASES  OF  THE  HEART 

disagreeable  sensation  evoked  when  lie  attempts  to  perform  some  act  which 
he  had  been  wont  to  do  with  ease,  and  without  distress.  Such  a  condition 
can  be  summed  up  as  due  to  the  too  speedy  exhaustion  of  the  reserve  force, 
and  manifested  by  a  limitation  of  the  field  of  cardiac  response.  The  sen- 
sations by  which  the  limitation  makes  itself  known  are  varied,  but  when 
carefully  analysed,  the  true  nature  of  the  heart  failure  is  revealed.  Hence, 
I  insist  upon  particular  attention  being  paid  to  the  patient's  sensations. 

The  standard  by  which  one  measures  the  strength  of  the  heart,  or,  more 
properly  speaking,  the  amount  of  the  reserve  force,  is  in  the  main  personal, 
as  each  individual  unconsciously  acquires  the  knowledge  of  what  he  can  do 
with  comfort,  and  his  attention  is  called  to  the  fact  that  his  range  of  effort 
has  become  circumscribed.  The  observing  physician  can  also  detect  signs 
in  the  frequent  pulse  and  quickened  respiration,  out  of  proportion  to  the 
exertion.  Other  sources  of  information  are  obtained  from  the  physical 
examination  of  the  patient,  not  only  in  the  heart  itself,  but  in  the  condition 
of  the  circulation  in  other  organs  and  tissues,  as  well  as  in  the  reflex  protective 
phenomena  which  appear  in  affections  of  the  heart  as  in  affections  of  other 
viscera. 

§  7.  Methods  adopted  in  describing  affections  of  the  heart. — The 
ideal  method  in  writing  a  book  on  diseases  of  the  heart  would  be  to  take  up 
each  separate  lesion,  and  describe  the  symptoms  that  arise  in  consequence 
of  the  lesion.  But  although  this  method  is  the  one  that  has  been  attempted 
by  most  writers  of  textbooks,  it  is  impracticable  in  our  present  state  of 
knowledge.  Not  only  are  the  lesions  imperfectly  recognized,  but  the  symp- 
toms themselves  are  usually  not  the  outcome  of  the  organic  lesion,  but  result 
from  the  embarrassment  of  the  heart  induced  by  the  lesion.  Thus  the 
symptoms  of  heart  failure  in  a  case  of  valvular  disease  are  not  produced 
by  the  valve  lesion,  but  by  the  failure  of  the  heart  muscle  to  overcome  the 
difficulty  created  by  the  damaged  valve,  and  this  failure  may  be  brought 
about  in  a  variety  of  ways  by  the  greater  exhaustion  of  one  function  than 
of  another, — sometimes,  for  example,  it  is  the  contractile  power  of  the  heart 
that  gives  way,  sometimes  the  tonicity  ;  so  that  we  get  a  variety  of  symp- 
toms corresponding  to  the  exhaustion  of  different  functions.  But  these 
functions  may  become  exhausted  from  other  causes  than  valvular  lesions, 
and  similar  symptoms  may  therefore  be  induced  by  organic  lesions  of  great 
diversity.  Another  reason  for  not  following  this  ideal  method  is  that  it 
is  extremely  rare  that  the  heart  is  the  seat  of  only  one  lesion,  or  of  a  lesion 
limited  to  one  particular  part.  Acute  affections  of  the  heart,  for  instance, 
are  often  described  as  endocarditis  or  pericarditis,  because  there  happens 
to  be  a  marked  systohc  murmur  or  a  pericardial  friction  sound.     But  in 


GENERAL  OUTLINE  OF  HEART  FAILURE  6 

addition  to  these  audible  signs,  there  may  be  presented  a  great  number  of 
symptoms  such  as  dilatation  of  the  heart,  irregular  action  of  the  heart, 
and  so  forth,  and  these  are  given  as  being  symptoms  of  the  endocarditis  or 
pericarditis.  As  a  matter  of  fact,  these  symptoms  are  not  the  outcome 
of  endocarditis  or  pericarditis,  but  of  a  myocardial  affection,  and  the  attempt 
to  give  a  precise  description  of  the  symptoms  pertaining  to  each  organic 
lesion  has  led  writers  to  ascribe  phenomena  to  lesions  with  which  they  have 
no  connexion,  with  the  result  that  the  symptomatology  of  heart  affections 
is  to-day  confused  and  contradictory. 

In  searching  for  a  reason  for  this  confusion,  I  am  incUned  to  attribute 
it  to  the  fact  that  the  human  mind  attaches  the  greatest  importance  to  that 
class  of  phenomena  which  most  strongly  affects  the  senses.  Many  of  the 
really  vital  and  aU-important  symptoms  are  so  subtle  and  so  shght  that  it 
takes  the  most  careful  methods  to  detect  them,  whereas  a  roaring  murmur 
or  an  irregular  pulse  thrusts  itself  upon  our  attention.  The  result  is  that 
the  subtle  signs  are  ignored  and  aU  the  stress  is  laid  upon  the  murmur  and 
irregularity.  Murmurs  and  irregularities,  therefore,  have  come  to  occupy 
a  far  more  important  place  in  the  cardiac  symptomatology  than  their  true 
significance  merits. 

These  considerations  have  led  me  to  adopt  a  method  which  I  hope  will 
place  the  symptoms  in  a  proper  perspective.  Recognizing  the  fact  that  the 
attention  of  the  physician  or  the  patient  is  drawn  to  the  heart  by  the  appear- 
ance of  one  or  more  symptoms — and  it  is  only  by  the  recognition  of  the 
symptoms  that  the  diseases  can  be  inferred, — I  write  this  book  from  the 
standpoint  of  the  symptoms.  So  far  as  I  can,  I  describe  each  symptom, 
give  its  physiological  meaning,  and  the  various  pathological  conditions 
with  which  it  may  be  associated.  Then  I  try  to  estimate  its  significance. 
From  the  data  thus  obtained,  conclusions  are  drawn  as  to  prognosis  and 
treatment. 


CHAPTER  II 

Fundamental  Functions  of  the  Heart  Muscle-cells 

§   8.  ]Myogenic  doctrine. 

9.  Stimulus  production. 

10.  Excitability. 

11.  C'onducti%'ity. 

12.  Contractility. 

13.  Tonicity. 

14.  Co-ordination  of  functions. 

15.  Characteristics  of  the  functions  of  the  heart  muscle-fibres. 

§  8.  Myogenic  doctrine. — While  it  would  be  somewhat  beyond  my 
province  to  enter  into  a  discussion  of  the  question  whether  the  heart  contracts 
in  response  to  a  nerve  stimulus,  or  in  response  to  a  stimulus  developed  in  the 
muscle-cells,  it  is  very  necessary,  in  order  to  comprehend  the  meaning  of 
the  signs  and  symptoms  that  arise  in  affections  of  the  heart,  to  appreciate 
the  phenomena  which  are  associated  with  the  contraction  of  the  muscle- 
fibres.  The  conception  of  the  meaning  of  the  heart  beat,  which  we  owe  to 
Gaskell,  has  been  supported  by  careful  and  minute  analysis  of  the  functions 
of  the  normal  heart  muscle-fibres,  and  the  interpretation  of  the  symptoms 
of  heart  affections  in  the  light  of  this  knowledge  has  revealed  so  clearly 
their  true  meaning  as  to  revolutionize  the  study  in  the  human  subject. 
Even  if  the  '  Myogenic  doctrine  '  be  ultimately  proved  untenable,  the 
investigations  carried  out  in  its  support  have  added  so  much  of  value 
to  our  knowledge  of  the  heart's  action  that  its  conception  will  ever  be 
associated  with  a  great  stride  forward,  not  only  in  physiology,  but  also  in 
the  recognition  and  treatment  of  diseases  of  the  heart.  It  is  just  possible 
that  the  two  opposing  doctrines — Neurogeny  and  Myogeny — may  be 
reconciled  along  the  lines  I  suggest  in  the  following  brief  summary  of  the 
main  points.  I  do  not  enter  into  much  detail,  but  give  such  salient  points 
as  are  necessary  to  appreciate  the  explanation  of  the  symptoms  I  give  in 
the  course  of  this  work.  For  fuller  details  the  reader  is  referred  to  Gaskell's 
article  on  '  The  Contraction  of  the  Cardiac  Muscle  '  in  Schaefer's  Text  Book 
of  Physiology. 

From  the  consideration  of  the  physiology  of  the  cell,  it  may  be  said 
that  every  function  possessed  by  a  cell  in  the  fully  developed  state  exists 
partiallj'  developed  in  the  primitive  form.    However  specialized  the  function 


FUNDAMENTAL  FUNCTIONS  OF  THE  HEART  MUSCLE-CELLS  7 

may  be,  nervous,  muscular,  or  secretory,  these  functions  can  be  referred 
back  to  some  property  possessed  by  the  primitive  cell.  The  cells  which  con- 
stitute the  primitive  structure  of  the  body  all  start  equally  endowed,  and 
it  is  by  a  gradual  process  of  specialization  that  each  takes  on  its  peculiar 
function,  while  as  it  acquires  a  high  degree  of  speciahzation  it  gradually 
loses  those  functions  it  no  longer  exercises.  The  functions  possessed  by  the 
primitive  cells  can  therefore  be  deduced  not  only  from  the  results  of  direct 
observation,  but  from  the  specialized  functions  of  the  more  differentiated 
tissues,  even  if  these  functions  be  so  highly  developed  that  they  bear  little 
resemblance  to  those  found  in  the  primitive  cell.  For  instance,  the  excita- 
bihty  of  the  cell  may  become  so  specialized  as  to  be  responsive  only  to  certain 
stimuli,  as  heat,  pain,  light,  sound,  while  all  its  other  functions  are  appa- 
rently lost.  If  one  looks  at  the  functions  of  nerve  and  muscle  cells  in  the 
fully  developed  state,  it  seems  at  first  sight  difficult  to  realize  that  they  had 
originally  identical  functions.  The  primitive  cells,  from  which  the  heart 
developed,  had  all  the  same  characteristics,  yet  in  their  final  evolution 
they  present  widely  divergent  characteristics  both  in  appearance  and  in 
function.  That  some  such  modification  does  occur  must  be  inferred  when 
we  witness  the  change  in  function  that  takes  place  in  the  evolution  of  the 
heart  from  the  primitive  cardiac  tube.  I  therefore  suggest  as  a  working 
hjrpothesis,  that  in  the  evolution  of  the  heart  muscle-fibres  certain  functions 
of  the  primitive  cell  were  retained,  some  of  these  being  more  developed  than 
others  according  to  the  duties  the  fibres  had  to  perform,  so  that  while  they 
have  come  to  resemble  muscle-fibres,  they  nevertheless  retain  in  a  varying 
degree  some  functions  which  are  highly  specialized  in  the  nerve-cell. 

The    special    functions   which   Gaskell   has   demonstrated   are  five    in 
number,  namely  : — 

(1)  The  power  of  producing  a  stimulus  which  can  excite  the  heart  to 

contract — stimulus  production. 

(2)  The  power  of  being  able  to  receive  a  stimulus — excitability. 

(3)  The  power  of  conveying  a  stimulus  from  fibre  to  fibre — conductivity. 

(4)  The  power  of  contracting  when  stimulated — contractility. 

(5)  The  power  to  retain  a  certain  amount  of  contraction  even  when 

the  active  movement  has  ceased — tonicity. 

§  9.   Stimulus  production From  this  point  of  view  it  is  assumed  that 

the  heart  muscle-fibres,  if  suppHed  with  appropriate  nutriment,  possess 
a  power  of  internally  secreting  a  material  which  is  capable  of  stimulating 
the  fibre  to  contract.  This  material  is  being  continually  secreted,  and  during 
a  pause  in  the  heart's  contraction,  accumulates  in  the  heart  cell.  When 
sufiicient  has  been  stored  to  excite  the  heart  to  contract,  the  whole  store 


8  DISEASES  OF  THE  HEART 

is  used  up  in  stimulating  the  muscle-cell.  Immediately  after  the  contraction 
the  store  again  begins  to  accumulate  until  sufficient  has  been  produced 
to  excite  the  heart  to  further  contraction.  This  function,  being  continuous 
in  its  action,  cannot  control  the  rhythm  of  the  heart,  but  by  its  co-operation 
with  the  other  functions  a  rhythmical  character  is  given  to  the  accumu- 
lation and  destruction  of  this  material. 

§10.  Excitability. — The  heart  muscle  depends  for  its  contraction  upon 
its  power  of  receiving  a  stimulus — that  is,  upon  its  excitabiUty.  Imme- 
diately after  the  heart  has  been  stimulated  to  contract,  the  fibres  are  no 
longer  capable  of  further  stimulation,  excitability  has  disappeared,  and  the 
fibres  are  in  what  is  called  the  refractory  stage.  The  excitability  begins 
at  once  to  be  restored,  and  increases  very  rapidly  during  diastole.  This  is 
demonstrated  by  the  heart  being  susceptible  to  weaker  stimuli  the  longer 
the  time  since  the  previous  contraction.  So  long  as  the  heart  is  capable  of 
contracting,  the  rate  of  the  heart  depends  upon  the  functions  of  stimulus 
production  and  excitability,  and  when  the  conditions  are  normal  the  equal 
action  of  both  functions — the  stimulus  material  being  renewed  at  a  uniform 
rate,  and  the  restoration  of  the  excitability  taking  place  uniformly — a  regular 
rhythm  of  the  heart's  action  results.  Under  normal  circumstances,  therefore, 
the  heart's  rate  and  rhythm  are  dependent  upon  the  integrity  of  these  two 
functions. 

§  II.  Conductivity. — In  a  mass  of  primitive  cells  the  individual  cell 
has  a  power  of  passing  the  stimulus  on  to  neighbouring  cells.  This  function 
of  conductivity  is  possessed  by  the  heart  muscle-fibres,  for  the  stimulus 
is  passed  on  from  ceU  to  cell  from  the  point  where  it  originated.  The 
possession  of  this  function  by  the  muscle-fibres  of  the  heart  gives  them 
a  character  which  is  typical  of  certain  forms  of  nerve-fibres,  but  in  the  heart 
this  is  not  so  highly  developed  as  in  the  speciaUzed  nerve-fibre,  the  conduction 
of  the  stimulus  not  being  so  rapid  in  all  cases,  andmuch  more  easily  exhausted. 
Like  every  other  function  of  the  heart,  it  is  entirely  abolished  after  it  has 
been  exercised,  and  it  returns  gradually.  The  rate  an  impulse  travels  also 
varies  in  different  fibres  of  the  heart.  Some  fibres,  such  as  the  more  recently 
developed  contractile  fibres  of  the  auricle  and  ventricle,  conduct  the  stimulus 
with  much  greater  rapidity  than  the  fibres  which  convey  the  stimulus  from 
auricle  to  ventricle. 

§  12.  Contractility — The  power  of  contraction  is  the  most  evident 
of  all  the  functions  of  the  heart.  By  the  co-ordinated  contraction  of  the 
fibres  of  the  different  portions  of  the  heart,  the  circulation  is  maintained. 
After  a  contraction,  this  function  is  completely  exhausted,  and  the  power 
returns  very  gradually.    Within  certain  limits  the  strength  of  the  contraction 


FUNDAMENTAL  FUNCTIONS  OF  THE  HEART  MUSCLE-CELLS  9 

depends  upon  the  length  of  the  period  of  rest  preceding  the  contraction, 
the  function  gathering  strength  during  quiescence. 

§  13.  Tonicity. — The  functions  of  the  heart  muscle  do  not  differ, 
except  in  degree,  from  those  of  other  muscular  structures,  and  as  tone  is 
a  very  characteristic  property  of  muscular  tissue,  it  is  certain  that  the  heart 
muscle  will  possess  it,  and  it  is  shown  by  the  fibres  not  relaxing  to  their  full 
length  during  diastole.  On  account  of  the  rapid  action  of  the  heart  it  is 
not  easy  to  demonstrate  this  function.  Gaskell^"'  has  shown  that  the  degree 
of  relaxation  depends  on  the  amount  of  tone  present,  and  that  certain  drugs 
increase  or  diminish  the  amount  of  relaxation.  Thus  antiarin,  veratrin,  and 
digitalis  prevent  the  relaxation  of  the  heart  muscle  in  the  frog  so  that 
the  heart  remains  longer  in  the  condition  of  complete  contraction,  the 
relaxation  gradually  becoming  less  and  less,  till  finally  it  is  almost  impossible 
to  recognize  individual  beats.  On  the  other  hand,  solutions  of  lactic  acid 
and  muscarin  produce  the  opposite  effect,  the  heart  becoming  more  and 
more  relaxed,  the  contraction  diminishing  in  size  till  the  heart  stands  still 
in  diastolic  relaxation.  Just  as  certain  portions  of  the  musculature  have 
certain  functions  more  highly  developed,  it  would  not  be  unreasonable,  as 
Gaskell  says,  to  expect  that  different  parts  of  the  heart  should  vary  in  their 
tonicity.  That  this  expectation  is  justified  will  be  manifest  when  all  the 
symptoms  of  heart  failure  are  considered,  and  it  is  only  on  recognizing  that 
the  heart  possesses  this  very  important  function  that  we  can  understand 
some  of  the  most  significant  features  of  heart  failure. 

§  14.  Co-ordination  of  functions When  the  complicated  action  of 

the  heart  is  considered,  it  will  be  readily  recognized  that  though  all  the 
fibres  may  be  endowed  Avith  these  functions,  a  further  speciahzation  is 
a  necessity  for  the  co-ordinated  movement  of  the  different  parts  of  the 
heart.  If  all  the  fibres  were  equally  endowed,  then  all  would  contract 
simultaneously.  As  it  is,  certain  fibres  at  the  venous  end  have  the  functions 
of  stimulus  production  and  excitability  more  highly  developed  than  others, 
so  that  after  a  period  of  rest  the  contraction  starts  in  them.  The  stimulus 
then  proceeds  to  adjoining  fibres  in  such  a  manner  that  the  process  of 
stimulation  and  contraction  sweeps  through  the  whole  heart,  with  the 
result  that  the  different  chambers  and  the  different  parts  of  each  chamber 
contract  in  that  order  and  degree  necessary  to  the  efficient  carrjang  on  of 
the  circulation.  If  anj^  other  part  of  the  heart  be  rendered  more  excitable 
than  the  venous  end,  then  the  contraction  starts  there.  As  the  stimulus 
then  does  not  sweep  through  the  heart  in  the  normal  manner,  the  heart's 
action  is  less  efficient,  and  heart  failure  may  thus  arise. 

§  15.  Characteristics  of  the  functions  of  the  heart  muscle-fibres. — 


10  DISEASES  OF  THE  HEART 

While  the  heart  may  be  said  to  carry  on  its  work  in  consequence  of  its  pos- 
session of  these  functions,  there  are  other  important  features  in  each  which 
have  a  practical  bearing  on  the  symptoms  of  diseases  and  the  principles 
of  treatment.  The  integrity  of  these  functions  depends  on  the  supply  of 
suitable  nutriment,  and  sufficient  time  of  inactivity  to  recover  after  their 
exercise.  When  a  contraction  takes  place,  all  the  functions  have  been  exer- 
cised to  the  full  extent  of  the  power  possessed  by  the  fibres  at  the  moment 
of  stimulation.  No  heart-cell  exhausts  only  a  portion  of  its  function  ; 
when  stimulated,  it  uses  all  the  energy  which  it  possesses  (all  or  nothing). 
For  a  brief  period  after  their  exercise,  the  functions  cease  to  exist :  recovery, 
however,  begins  at  once  during  the  period  of  rest,,  and  each  function  in  time 
regains  its  strength,  so  that,  within  certain  limits,  the  longer  the  delay,  the 
more  complete  is  the  recovery,  and  the  more  efficient  is  the  subsequent 
action.  It  is  by  fully  appreciating  the  effect  of  rest  and  proper  nourishment 
that  we  gain  the  best  conception  of  the  principle  that  should  underlie  our 
treatment  of  heart  failure.  While  all  the  functions  when  exercised  use  all 
the  force  they  possess,  they  nevertheless  manifest  a  quaUty  whereby  they 
can  respond,  under  certain  circumstances,  with  a  greater  activity.  Thus 
the  rate  may  be  suddenly  increased,  and  at  the  same  time  the  stimulus 
passed  from  the  auricle  to  the  ventricle  with  increased  rapidity,  and  the 
contraction  be  executed  quicker.  These  changes  are  to  a  great  extent 
under  the  control  of  the  nervous  system,  but  they  imply  a  quaUty  possessed 
by  aU  these  functions  which  is  of  vital  importance  to  us  in  the  study  of  heart 
failure.  For,  as  I  have  already  remarked,  it  is  this  power  of  responding 
to  effort  that  gives  us  the  clue  to  the  real  state  of  the  heart. 

When  one  reflects  that  aU  the  fibres  of  the  heart  are  not  equally  endowed 
with  the  same  functions,  and  that  aU  the  functions  may  not  always  be 
exposed  to  an  equal  strain,  it  is  but  reasonable  to  conclude  that  conditions 
may  arise  where  they  are  unequally  affected.  As  a  matter  of  fact,  this  is 
what  commonly  happens,  and  it  is  an  interesting  and  important  question 
to  consider  in  each  case  of  heart  failure  what  functions  are  specially  at  fault. 
The  significance  of  this  question  was  demonstrated  when  Wenckebach-^ 
showed  how  the  irregular  activity  of  the  various  functions  or  of  the  various 
parts  of  the  heart  were  made  manifest  by  certain  characteristic  arrhythmias. 
Following  up  the  idea  of  exhaustion  or  over-excitability  of  individual  func- 
tions, I  have  sought  to  connect  many  of  the  symptoms  of  heart  failure 
with  these  functions.  While  I  do  not  say  that  my  conclusions  are  invariably 
correct,  they  have  led  to  some  definite  results  of  the  very  highest  importance, 
and  it  is  along  these  lines  that  advance  in  our  knowledge  will  likely  follow 
for  some  time. 


CHAPTER  III 

Development,  Anatomy,  and  Physiology  of  the  Heart 

§   16.  The  primitive  cardiac  tube. 

17.  The  functions  of  the  primitive  cardiac  tube. 

18.  The  remains  of  the  primitive  cardiac  tube  in  the  mammaUan  heart. 

19.  Functions  of  the  primitive  cardiac  tissue  in  the  mammalian  heart. 

20.  Functional  anatomy  of  the  heart. 

21.  The  nerve  supply  of  the  heart. 

While  I  take  it  for  granted  that  the  reader  is  f amiHar  with  tlie  ordinary 
textbook  description  of  the  anatomy  and  physiology  of  the  heart,  there  are 
some  recent  investigations  which  have  an  important  bearing  on  the  cUnical 
investigation  of  heart  disease  which  need  to  be  considered.  For  that  reason 
I  give  here  a  brief  resume  of  certain  points  necessary  for  the  appreciation  of 
chnical  signs. 

§  1 6.  The  primitive  cardiac  tube — In  an  early  stage  of  the  embryo's 
development,  the  heart  appears  as  a  tube.  The  veins  from  the  body  unite 
into  a  common  cavity — the  sinus  venosus — at  the  posterior  end  of  this  tube. 
In  the  course  of  development  this  tube  becomes  bent  upon  itself,  and  from 
it,  later,  pouches  develop  which  ultimately  become  the  auricles  and  ventricles 
— the  original  tube  still  persisting  and  connecting  them  (Fig.  1).  As  develop- 
ment proceeds,  the  sinus  venosus  loses  its  distinctive  feature  as  a  separate 
structure  to  become  incorporated  in  the  termination  of  the  superior  and 
inferior  vena  cavae,  and  a  strip  of  the  right  auricle  between  the  orifices  of 
those  two  vessels,  and  the  coronary  sinus.  Probably  the  terminal  part  of 
the  pulmonary  veins  is  also  derived  from  the  sinus.  At  the  same  time  the 
original  cardiac  tube  ceases  to  exist  as  a  tube  but  it  is  inferred  that  it  persists 
as  the  connecting  medium  between  auricles  and  ventricles  in  the  shape 
of  a  band  of  pecuHar  fibres — the  a.-v.  bundle  (Fig.  2).  It  thus  loses  its 
function  as  a  propelling  organ,  which  is  taken  up  by  the  auricles  and 
ventricles. 

§  17.  The  functions  of  the  primitive  cardiac  tube. — The  functions 
of  the  primitive  cardiac  tube  and  its  representative  in  the  mammalian  heart 
need  to  be  carefully  studied,  as  the  appreciation  of  the  nature  of  its  functions 
has  the  most  important  bearing  on  many  cases  of  heart  failure.  Its  pecuUar 
properties  have  been  studied  most  fully  in   the  heart    of   the  frog,  also 


12 


DISEASES  or  THE  HEART 


in  the  toad,  tortoise,  crocodile,  &c.,  but,  so  far,  only  to  a  slight  extent  in 
the  mammalian  heart.  In  the  lower  vertebrates  the  primitive  tube  is  still 
recognizable  in  the  sinus  venosus,  auricular  canal,  and  aortic  bulb  (Fig.  1). 
It  has  been  found  that  the  posterior  end  of  this  tube  is  the  most  excitable 
portion,  and  in  consequence  of  this  the  heart's  contraction  starts  at  the  sinus 
venosus.  The  remainder  of  the  tube  also  possesses  the  faculty  of  starting 
the  heart's  contraction,  only  in  a  less  degree  than  the  sinus.  If,  how- 
ever, any  part  of  the  tube  be  rendered  more  excitable  than  the  sinus  the 


Auricle, 
I 


Auricular  part  of 
primitive  cardiac  tute. 


Aorta. 

Bulbar  part  of  primitive 
cardiac  tube,  included  in 
liuman  right  ventricle. 

Bnlbus  cordis. 


^^vV    _  Ventricular  part  of 

primitive  cardiac  tube. 


Inferior  vena  cava. 


Fig.  1.  Diagram  of  the  primitive  vertebrate  heart,  showing  the  development  of  the  auricle 
and  ventricle  from  the  primitive  cardiac  tube.      (Keith.) 


contraction  starts  from  that  part.  The  pecuharity  of  the  primitive  cardiac 
tube  and  its  relatively  greater  excitability  than  the  auricular  or  ventricular 
tissue  is  brought  out  in  the  following  experiment  by  GaskeU  ^-^ :  '  Touch 
the  auriculo-ventricular  ring  of  muscle  (i.e.  the  primitive  cardiac  tube) 
with  the  sUghtest  stimulus,  immediately  a  series  of  rhythmical  contractions 
occurs.  It  is  most  striking  to  see,  after  removal  of  the  septum,  how 
every  portion  of  auricular  and  ventricular  tissue  can  be  explored  up  to  the 
very  edge  of  the  ring,  without  obtaining  more  than  a  single  contraction, 
while  immediately  the  needle  touches  the  muscular  ring  a  series  of  rapid 
contractions  results.' 

The  possession  of  the  power  of  independent  contraction  by  the  separate 


DEVELOPMENT,  ANATOMY,  AND  PHYSIOLOGY  13 

portions  of  the  heart  is  brought  out  in  the  Stannius  experiments.  When 
a  ligature  is  apphed  or  a  cut  made  between  the  sinus  and  auricle  of  a  frog's 
heart  {A,  Fig.  1),  so  as  to  sever  completely  the  connexion,  the  sinus  con- 
tinues beating,  and  after  a  pause  of  varying  duration  the  auricles  and 
ventricles  begin  to  beat  at  a  rate  different  from,  and  independent  of,  the 
sinus.  This  rate  is  slower  than  the  sinus  rate,  and  sometimes  the  auricle 
contracts  before  the  ventricle,  sometimes  the  ventricle  precedes  the  auricle, 
and  very  rarely  they  contract  simultaneously.     (Engelmann  ^^^). 

If  a  second  Stannius  hgature  be  apphed  between  auricle  and  ventricle 
{B,  Fig.  1),  the  sinus  and  auricle  continue  beating,  and  after  a  period  the 
ventricle  takes  on  its  own  rhythm,  slower  than,  and  independent  of,  the 
other  portion  of  the  heart. 

§  1 8.  The  remains  of  the  primitive  cardiac  tube  in  the  mamma- 
lian heart. — The  sinus  venosus,  which  in  the  primitive  heart  normally  origi- 
nated the  stimulus  for  contraction,  has  no  representative  as  an  independent 
structure  in  the  human  heart.  Morphologists  recognize  that  it  has  become 
incorporated  in  the  great  veins  near  the  heart,  and  physiologists  observed 
that  the  peculiar  functions  of  the  sinus  venosus  were  found  over  a  somewhat 
wide  distribution.  Normally,  the  contraction  starts  with  such  uniformity 
in  a  number  of  places  that  no  one  place  can  be  pointed  out  with  certainty 
as  the  starting-point,  though  the  mouth  of  the  superior  vena  cava  seems  to 
lead  the  contraction.  In  certain  experiments  dissociation  can  be  shown,, 
and  independent  pulsations  start  at  the  coronary  sinus  and  pulmonary  veins. 
From  this  it  is  inferred  that  in  these  separate  places  some  remains  of  the 
original  sinus  venosus  persist,  the  possession  of  which  endows  them  with 
the  power  of  starting  independent  contractions.  Until  very  recent  times 
no  definite  remains  of  the  sinus  venosus  had  been  found.  Keith  and  Flack  ^-^ 
have  described  lately  a  small  node  of  tissue — the  sino-auricular  node 
(1,  Fig.  2) — at  the  mouth  of  the  superior  vena  cava.  This  tissue  consists  of 
fine  delicate  pale  fibres  faintly  striated,  in  which  branches  of  the  vagus  and 
sympathetic  nerves  terminate,  and  is  suppHed  with  a  definite  artery.  These 
observers  consider  that  this  node  of  tissue  represents  a  portion  of  the  sinus 
venosus,  from  which,  probably,  the  heart's  contraction  starts.  Similar 
tissue  has  so  far  not  been  found  in  the  other  veins.  It  is  possible  that  some 
fibres  may  be  scattered  about,  but,  not  being  grouped  into  a  definite  node, 
they  are  not  capable  of  being  differentiated  from  the  muscular  fibres  by 
which  they  are  surrounded.  The  further  remains  of  the  primitive  cardiac 
tissue  are  probably  found  lower  down,  arising  in  the  right  auricle  and  passing 
across  the  a.-v.  septum  to  be  distributed  inHhe  ventricles.  Although  the 
presence  of  this  bridge  was  inferred  in  the  mammalian  heart  by  Gaskel,  it 


14  DISEASES  OF  THE  HEART 

was  not  demonstrated  until  1893,  when  first  Stanley  Kent^^^,  then  His 
( j  unr . )  -^^,  described  its  presence  and  both  experimentally  demonstrated  some  of 
its  functions.  A  full  description  of  its  structure  and  ramification  was  given 
in  1906  by  Tawara^-^  whose  elaborate  examination  of  the  tissue  has  been 
of  the  greatest  interest  and  importance.  This  bundle  rises  from  a  node  of 
tissue — the  a.-v.  node  (2,  Fig.  2) — situated  in  the  right  auricular  wall  near 
the  mouth  of  the  coronary  sinus,  and  Colin -^"^  has  recently  worked  out  some 
of  the  details  connecting  it  with  the  muscle-fibres  of  the  auricle.  The  bundle 
passes  over  the  auriculo-ventricular  septum  below  the  central  fibrous  body 
and  under  the  septal  cusp  of  the  tricuspid  valve.  While  on  the  septum 
it  divides  into  two,  one  branch  passing  into  the  left  ventricle  and  the  other 
into  the  right.  In  the  right  ventricle  it  continues  its  course  as  a  narrow 
rounded  bundle  in  the  muscle-wall  of  the  heart,  till  it  approaches  the  apex, 
where  it  divides  into  numerous  fine  threads,  terminating  in  the  muscle- 
fibres.  In  the  left  ventricle  the  bundle  rapidly  widens  out  into  a  thin 
band  which  passes  down  to  the  apex  splitting  into  fine  branches. 

The  character  of  the  fibres  constituting  this  bundle  varies.  The  fibres 
of  the  a.-v.  node  are  of  the  same  delicate  nature  as  those  of  the  sino-auricular 
node.  As  this  bundle  passes  into  the  ventricle  the  fibres  change,  becoming 
thicker,  the  greater  part  of  the  cell  body  being  undifferentiated  protoplasm 
only  faintly  striated  at  the  circumference  and  containing  a  large  nucleus. 
In  their  final  distribution  they  are  recognized  as  being  the  fibres  described 
long  ago  by  Purkinje.  Another  pecuharity  of  this  bundle  is  that  it  is  isolated 
from  the  structures  in  which  it  is  embedded  by  a  fine  sheath  of  connective 
tissue.  There  are  numerous  nerve  structures  in  the  a.-v.  bundle  which  have 
been  specially  studied  by  Gordon  Wilson  ^^^.  He  finds  numerous  ganglion 
cells,  abundant  nerve-fibres,  an  intricate  plexus  around  the  muscle-fibres 
of  the  bundle,  and  distinct  vaso-motor  nerves.  Finally,  it  is  mainly  supphed 
by  a  special  branch  of  the  right  coronary  artery,  a  fact  of  some  significance 
in  the  pathology  of  the  heart. 

§  19.  Functions  of  the  primitive  cardiac  tissue  in  the  mammalian 
heart — The  functions  of  this  bundle  have  been  only  partially  explored 
experimentally,  though  a  fair  inference  of  its  functional  action  can  be  made 
from  clinical  symptoms.  Kent  ^°^,  His  (junr.)-^*^,  Erlanger  ^'^,  Hering  -'■'^,  and 
others  have  demonstrated  that  it  conveys  the  stimulus  from  auricle  to 
ventricle,  for  compression  of  the  bundle  interferes  with  the  conduction, 
while  section  stops  all  connexion,  and  the  ventricle  contracts  at  a  rate 
quite  independent  of  the  auricular  rate,  as  after  the  second  Stannius  ligature. 
An  exactly  similar  experience  is  met  with  as  a  result  of  disease  in  man. 

But,  as  has  been  seen,  the  primitive  cardiac  tube  also  possesses  the  power 


DEVELOPMENT,  ANATOMY,  AND  PHYSIOLOGY  15 

of  originating  the  stimulus  for  contraction,  and  there  is  every  reason  to  sup- 
pose that  if  it  be  rendered  more  excitable  the  remains  of  the  primitive  cardiac 
tissue  in  man  will  start  a  contraction  independent  of  the  sinus  rhythm.  In 
the  neighbourhood  of  the  node  there  are  certain  centres  which  when  stimu- 
lated modify  the  heart's  action.  Thus  Mac  William  ^'^^  has  shown  that  a  small 
area  in  the  auricle  here,  when  stimulated,  causes  marked  slowing  of  the 
ventricular  rate.    Whether  this  is  a  portion  of  the  vagus  mechanism  or  some 


Fig.  2.  Section  of  a  heart,  exposing  the  septal  wall  of  the  right  auricle  and  ventricle 
and  showing  the  position  of  a  portion  of  the  remains  of  the  primitive  cardiac  tube. 
1.  Superior  vena  cava  above  the  sino-auricular  node.  2.  Auriculo- ventricular  node  (Knoten 
of  Tawara),  from  which  the  auriculo-ventricular  bundle  arises.  The  interrupted  part 
represents  the  main  bundle,  and  the  continuation  to  3  is  the  right  division,  where  it  is  shown 
in  the  cut  moderator  band.  4.  Aorta.  5.  Right  auricle  below  the  sui^erior  caval  orifice  and 
taenia  terminaUs.     6.  Pulmonary  artery.     7.  Opening  of  coronary  sinus.     (Keith.) 

portion  of  the  primitive  cardiac  tissue  has  not  been  determined.  Lohmann  ^^", 
by  irritating  the  a. -v.  node,  or  its  immediate  neighbourhood,  caused  the 
starting  of  the  auricular  and  ventricular  contractions  together.  In  the 
human  subject  I  have  attempted  by  a  process  of  reasoning  to  show  that 
extra-systoles  may  arise  in  this  tissue,  and  that  the  continual  irregularity 
recognized  so  frequently  in  the  later  stages  of  rheumatic  heart  affection  and 
cardio-sclerosis,  may  be  due  to  the  inception  of  the  rhythm  of  the  heart  by 
the  irritated  primitive  cardiac  tissue  probably  in  or  about  the  a. -v.  node. 


16  DISEASES  OF  THE  HEART 

§  20.  Functional  anatomy  of  the  heart — I  mention  here  a  few  of 
the  more  important  features  connected  with  the  heart  as  a  muscular  organ 
which  are  of  importance  in  this  cKnical  study.  These  are  based  on 
Keith's  ^^*^  descriptions,  who  has  demonstrated  that  the  heart  is  built  of 
muscle  bundles  whose  points  of  origin  and  insertion  are  as  definite  as  those  of 
skeletal  muscles,  and  whose  functions  can  also,  to  a  great  extent,  be  inferred 
with  equal  certainty.  Naturally  the  separation  of  the  different  muscle 
bundles  is  not  so  complete  as  in  skeletal  muscles,  there  being  a  continuous 
connexion  between  neighbouring  fibres,  so  that  they  pass  gradually  from 
one  system  into  another. 

In  order  to  appreciate  how  the  muscle-fibres  act,  and  also  to  understand 
the  changes  that  result  from  an  increase  in  the  size  of  the  heart,  it  is  necessary 
to  comprehend  how  the  heart  is  fixed  in  the  thorax. 

The  pericardium  is  a  fairly  unyielding  structure  fixed  firmly  above 
to  the  cervical  fascia  and  below  to  the  central  tendon  of  the  diaphragm. 
The  aorta  and  the  great  veins,  where  they  penetrate  the  pericardial  sac, 
receive  a  covering  from  it,  and  these  may  be  regarded  as  fixed  points.  The 
lungs  also  may  be  considered  as  ligaments  which  attach  the  base  of  the 
heart  to  the  whole  of  the  chest-wall. 

The  contraction  of  the  heart  starts  at  the  mouth  of  the  great  veins.  It 
has  hitherto  been  assumed  that  regurgitation  from  the  auricle  was  prevented 
by  the  contraction  of  the  circular  fibres  at  the  mouth  of  the  veins.  Keith 
shows  that  these  are  too  weak  for  the  purpose,  except  around  the  coronary 
sinus,  and  that  regurgitation  back  into  the  superior  vena  cava  is  prevented 
by  the  contraction  of  the  broad  band  of  muscle  which  sweeps  over  the  roof  of 
the  auricle — the  taenia  terminalis.  In  its  contraction  this  muscular  band  shuts 
off  the  vein  from  the  auricular  cavity.  As  the  taenia  is  attached  at  the  orifice 
of  the  inferior  vena  cava  and  is  carried  over  the  roof  of  the  right  auricle,  it 
also  aids  in  the  closure  of  the  inferior  vena  cava  and  the  pulmonary  veins. 
The  pressure  of  the  blood  in  the  inferior  vena  cava  apparently  renders 
a  perfectly  competent  closure  of  the  inferior  caval  orifice  unnecessary. 

Arising  from  the  taenia  are  a  number  of  other  muscular  bands,  the 
pectinate  fibres,  which  pass  across  the  auricle  to  be  fixed  in  the  auriculo- 
ventricular  septum.  In  their  contraction,  in  addition  to  assisting  the  taenia 
in  emptying  the  auricle,  they  pull  up  the  ventricles  by  reason  of  their  insertion 
into  the  a.-v.  septum  {A,  Fig.  3). 

The  ventricles  have  themselves  no  real  fixed  point,  but  depend  for 
security  on  the  fixation  of  the  vessels  at  the  base  of  the  heart.  Immediately 
below  the  origin  of  the  aorta  in  the  heart  is  the  central  fibrous  body,  which 
is  reaUy  a  tendon  for  much  of  the  ventricular  muscle.     The  remainder  of 


DEVELOPMENT,  ANATOMY,  AND  PHYSIOLOGY 


17 


the  ventricular  muscle  is  inserted  into  the  a. -v.  septum.  The  other  fixed 
point  during  contraction  is  the  apex.  It  becomes  a  fixed  point  in  virtue 
of  the  peculiar  arrangement  of  the  muscles  here  constituting  the  '  whorl '. 
A  great  number  of  fibres  from  different  parts  of  the  heart  converge  here  and 


Fig.  3.  Sketch  of  the  heart  to  show  the  movements  of  the  auriculo- ventricular  gi'oove  during 
auricular  and  ventricular  systole.  A,  position  of  groove  when  pulled  upon  by  the  contraction 
of  the  pectinate  fibres  of  the  auricle  ;  B,  position  of  the  groove  when  pulled  upon  by  the  con- 
traction of  the  ventricular  fibres.  During  the  diastole  the  groove  occupies  a  position  midway 
between  A  and  B  ;  a,  sinus  portion  of  superior  vena  cava  ;  b,  inferior  vena  cava  ;  c,  is  on  the 
taenia  terminalis  ;  d,  apex  of  the  heart ;  /,  pulmonary  artery  ;  i,  i,  pulmonary  veins  ;  k,  pul- 
monary artery.  During  ventricular  systole  g'  is  pulled  to  g  and  e'  to  e  ;  h',  musculi  pectinati 
during  auricular  systole  ;   Ji",  during  ventricular  systole.     (Keith.) 

mutually  support  one  another  in  contraction,  the  result  being  a  fixed  point 
from  which  the  fibres  can  exercise  traction  in  different  directions.  With  the 
onset  of  the  ventricular  contraction  the  apex  of  the  heart  rises  up  and  presses 
firmly  against  the  chest-wall.  As  no  shortening  takes  place  between  the 
apex  and  the  aorta,  all  the  parts  of  the  heart  are  drawn  towards  the 
line  between  apex  and  aorta.     Hence  it  is  that  while  during  ventricular 

MACKENZIE  o 


18  ■  DISEASES  OF  THE  HEART 

contraction  the  apex  is  pushed  forwards,  all  the  other  portions  of  the  cardiac 
surface  are  dragged  inwards,  and  this  explains  the  variation  in  the  appear- 
ance of  a  cardiogram  taken  from  different  parts  of  the  front  of  the  chest. 
At  the  same  time,  as  Chauveau^^^  and  Keith  ^^^  have  shown,  the  ventricular 
fibres  inserted  into  the  a. -v.  septum  not  only  diminish  the  size  of  the  ven- 
tricle, but  enlarge  the  size  of  the  auricle  by  dragging  down  the  a.-v.  septum 
— a  fact  of  some  importance  in  the  production  of  the  venous  pulse  {B,  Fig.  3). 

§  21.  The  nerve  supply  of  the  heart — The  independent  functions 
of  the  muscle-fibres  enable  the  heart  to  execute  its  movements  independently 
of  any  nervous  intervention,  nevertheless  nervous  influences  have  a  powerful 
effect  in  modifying  the  activity  of  the  various  functions  of  the  fibres.  The 
nerves  of  the  heart  are  usually  described  as  being  of  three  sorts,  namely, 
(1)  inhibitory  fibres  passing  to  the  heart,  (2)  accelerator  or  augmentor 
fibres  also  passing  to  the  heart,  and  (3)  depressor  fibres  passing  from  the 
heart. 

The  inhibitory  fibres  are  derived  from  the  spinal  bulb  by  the  internal 
branch  of  the  spinal  accessory  nerve,  and  pass  down  in  the  vagus  and  reach 
the  heart  by  its  cardiac  branches.  The  effects  of  the  vagus  upon  the  heart 
are  varied.  On  division  of  one  vagus  little  effect  may  result.  If  both 
vagi  be  cut  the  frequency  of  the  heart  is  much  increased.  If  the  vagus  be 
stimulated  the  result  is  curiously  varied.  Its  action  may  be  said  in  a  general 
way  to  depress  the  functions  of  the  heart  muscle-fibres,  but  it  does  not  do 
so  uniformly  in  all  cases.  It  usually  acts  first  on  the  excitabihty  of  the 
heart  or  on  the  stimulus  production,  so  that  the  whole  heart  becomes  slower 
in  its  action,  or  the  whole  heart  may  stand  stiU  for  a  brief  period.  With 
stronger  stimulation,  it  may  act  on  the  conductivity  of  the  fibres  joining 
auricles  and  ventricles,  and  depress  this  function  so  that  the  ventricle  fails 
to  respond  to  every  auricular  systole.  Underlying  this  seemingly  uncertain 
action  of  the  vagus  is  a  principle  which  is  of  great  importance  in  diagnosis 
and  in  treatment,  namely,  that  if  there  be  depression  of  one  function  of  the 
heart,  vagus  stimulation  is  liable  to  seize  upon  that  function  and  increase  the 
depression.  The  fact  that  depressed  functions  are  more  susceptible  to  vagus 
stimulation  seems  to  be  the  reason  for  some  of  the  discordant  results  arrived 
at  by  experiments. 

The  accelerator  fibres  belong  to  the  sympathetic  system  and  have 
their  origin  in  the  spinal  cord,  passing  out  of  the  cord  by  the  white  rami 
communicantes  to  the  upper  four  or  five  dorsal  nerves.  They  pass 
upwards  to  the  inferior  cervical  ganglion  ;  from  thence  they  pass  to  join  the 
cardiac  fibres  of  the  vagus,  and  so  reach  the  heart.  Stimulation  of  these 
fibres  increases  the  rate  of  the  heart,  sometimes  very  considerably,  and 


DEVELOPMENT,  ANATOMY,  AND  PHYSIOLOGY  19 

according  to  Roy  and  Adami  ^"^  they  increase  the  strength  of  contraction 
and  output  as  well,  and  hence  have  been  assumed  to  contain  augmentor 
fibres. 

The  depressor  fibre  is  a  definite  nerve  which  arises  in  the  heart,  and,  pass- 
ing upwards,  joins  the  vagus  nerve  and  so  reaches  the  bulb.  Stimulation  of 
the  peripheral  part  of  the  cut  nerve  has  no  effect,  but  stimulation  of  the 
central  end  causes  a  fall  of  blood-pressure  through  reflex  action  on  the 
medulla  oblongata. 

Afferent  fibres. — Such  is  a  brief  resume  of  the  heart  nerves  described 
in  physiological  textbooks,  but  the  whole  matter  is  not  included  here. 
There  is  a  great  field  of  evidence  which  is  entirely  lost  to  the  physiologist, 
but  which  is  open  to  the  clinician.  The  personal  sensation  of  the  animal 
cannot  be  communicated  to  the  experimenter,  nor  can  the  changes  in  sensa- 
tion that  result  from  stimulation  of  the  cardiac  nerves  be  ascertained.  In 
dealing  with  the  symptoms  of  heart  affections  it  mil  be  shown  that  there 
is  unquestionable  evidence  of  a  system  of  nerves  passing  from  the  heart 
to  the  spinal  cord  and  the  bulb.  The  principles  involved  in  the  production 
of  these  symptoms  have  not  been  thoroughly  appreciated,  and  I  shall  enter 
more  fully  into  their  explanation  when  dealing  with  the  reflex  or  protective 
phenomena  (Chapter  VI). 

Cardiac  ganglion  cells. — The  nerve-fibres  of  the  a.-v.  bundle  have  been 
referred  to  on  p.  14.  The  ganglion  ceUs  in  the  heart  have  been  studied  by 
GaskeU  ^^^.  He  says,  '  WTiat,  then,  are  the  ganglion  cells  in  the  heart  ?  What 
function  do  you  attribute  to  them  ?  That  is  a  question  which  I  am  ready  to 
answer,  and  to  answer  with  confidence,  as  follows  :  The  gangUon  cells  in  the 
heart  are  part  of  the  great  group  of  ganglion  cells  which  are  situated  on  the 
course  of  the  small-fibred  efferent  nerves  supplying  the  viscera.  These  ceUs 
form  the  outlying  vagrant  groups  of  nerve-cells  which  are  known  by  the 
name  of  the  sympathetic  and  cerebro-spinal  gangha.  In  the  case  of  the 
heart,  the  ganglion  cells  are  the  cells  belonging  to  the  smaU-fibred  efferent 
cardiac  fibres  of  the  vagus,  just  as  some  of  the  cells  in  the  ganghon  stellatum 
and  in  the  inferior  cervical  ganglion  are  the  cells  belonging  to  the  small- 
fibred  efferent  cardiac  fibres  of  the  augmentor  nerve.  There  is  no  more  reason 
to  assign  special  functions  to  these  ceUs  than  to  any  of  the  other  peripheral 
efferent  nerve-cells.  They  are  cells  connected  only  with  the  inhibitory  fibres 
of  the  vagus,  and  as  such  are  simply  part  and  parcel  of  the  mechanism  of 
inhibition,  just  as  the  corresponding  cells  in  the  ganglion  stellatum  are 
simply  part  and  parcel  of  the  augmentor  mechanism.' 


c  2 


CHAPTER  IV 

Preliminary  Examination  of  the  Patient 

§  22.  The  patient's  appearance. 

23.  The  patient's  sensations. 

24.  The  patient's  history. 

25.  The  chief  complaints :    breathlessness,  sense  of  exhaustion,  pain,  constriction  of 

chest,    palpitation,    consciousness   of    irregular   action   of    the   heart,   haemor- 
rhages, cerebral  symptoms. 

§  22.  The  patient's  appearance — Before  entering  upon  the  physical 
examination  of  the  patient,  the  physician  ought  to  obtain  a  clear  and  com- 
prehensive appreciation  of  the  patient's  own  sensations.  I  therefore  wish 
to  insist  upon  the  importance  of  the  preliminary  examination,  for  it  often 
happens  that  a  thorough  appreciation  of  the  patient's  own  experiences  is 
of  more  value  in  arriving  at  a  correct  estimation  of  the  heart's  efficiency 
than  the  most  elaborate  methods  of  physical  examination.  The  attempt 
to  appreciate  the  patient's  condition  should  begin  when  first  he  presents 
himself  before  us.  On  his  appearance  in  the  consulting-room,  his  bearing, 
his  gait,  the  condition  of  his  respiration,  the  colour  of  his  face,  any  nervous 
peculiarity  in  his  manner  of  speech  and  behaviour,  and  so  forth,  should 
be  noted.  If  he  is  in  bed,  note  the  position  he  assumes,  and  any  change 
in  his  colour  or  respiration  in  response  to  such  exertions  as  talking  or 
turning  over.  By  habit,  one  unconsciously  notices  these  things,  and  as  the 
examination  proceeds  first  one  trivial  matter,  then  another,  may  arise, 
which  helps  materially  in  guiding  the  examination  and  in  forming  the 
final  opinion. 

§  23.  The  patient's  sensations. — After  ascertaining  his  age  and  occu- 
pation, ask  the  patient  to  describe  the  chief  symptoms  from  which  he  suffers. 
In  his  replies,  insist  upon  these  being  precise  and  definite.  When  he  refers 
to  his  feelings,  get  him  to  indicate  the  location  by  placing  his  hand  upon  the 
region  ;  otherwise,  proud  of  his  small  anatomical  knowledge,  he  will  attribute 
his  sensations  to  his  viscera ;  and  here  I  may  add  a  warning  to  the  physician 
not  to  make  a  note  of  the  sensations  by  attributing  them  to  any  viscus  : 
thus  a  pain  should  not  be  put  down  as  felt  in  the  heart,  stomach,  liver,  or 
lungs,  but  only  in  the  region  of  the  body  indicated  by  the  patient,  for 
it  will  probably  be  found  on  later  examination  that  the  pains  are  not  felt 


PRELIMINARY  EXAMINATION  OF  THE  PATIENT  21 

in  the  viscus.  In  other  words,  he  should  make  no  notes  that  might 
prejudge  the  nature  of  any  symptom  until  he  has  before  him  all  the 
evidence. 

Having  obtained  from  the  patient  an  account  of  the  symptoms  from 
which  he  suffers,  a  brief  inquiry  should  be  made  regarding  the  other  viscera, 
as  to  the  state  of  the  digestion,  the  urinary  secretion,  the  breathing,  &c. 
Particular  inquiries  should  always  be  made  in  regard  to  sleep,  for  in  many 
patients  the  want  of  sleep  induces  a  breakdown,  and  the  power  of  a  patient 
to  pass  a  night  in  comfort  or  otherwise,  often  gives  important  indications. 
The  condition  of  the  brain,  its  power  of  attention,  memory,  dreams,  and  so 
forth,  are  often  of  material  value. 

§  24.  The  patient's  history — After  this,  I  usually  inquire  into  the  past 
history  for  other  illnesses,  the  nature  of  employment,  whether  there  is  worry, 
excessive  indulgence  in  tobacco  or  alcohol.  Guided  by  the  information  thus 
obtained,  I  return  again  to  the  main  complaints,  and  inquire  when  they 
began  to  appear,  and  what  induced  their  appearance.  In  all  cases  it  is 
necessary  to  find  out  what  degree  of  exertion  the  patient  can  undertake 
with  comfort.  As  I  have  said,  heart  failure  resolves  itself  into  the  question 
of  the  amount  of  reserve  force,  and  consequently  it  is  at  this  juncture  that 
we  begin  to  find  out  that  amount ;  therefore  the  factors  that  produce  the 
first  sign  of  discomfort  need  the  most  detailed  inquiry.  The  sequence  of 
the  phenomena  as  they  arise  is  most  instructive.  The  patient  has  often 
only  a  confused  notion  of  the  order  of  appearance  of  the  sensations,  and  the 
situation  in  which  they  are  felt,  and  it  may  be  necessary  to  postpone  a  final 
opinion  until  a  second  visit,  and  the  patient  should  be  instructed  to  note, 
should  occasion  arise,  the  individual  sensations,  their  location,  and  order 
of  appearance.  On  a  subsequent  visit  the  account  may  be  totally  different, 
but  often  one  made  with  great  precision.  It  is  sometimes  surprising  to 
observe  that  a  patient,  after  an  attack  of  agonizing  pain,  has  but  a  very 
dim  idea  in  what  region  it  was  felt.  Inquiries  should  be  made  as  to  the 
presence  of  less  obtrusive  symptoms,  which  experience  tells  us  to  expect,  but 
which  the  patient  often  ignores,  unless  his  attention  is  drawn  to  them.  Thus 
when  he  complains  of  a  pain  in  the  chest,  is  it  associated  with  a  sense  of 
constriction,  or  after  it  passes,  is  there  a  desire  to  micturate  ?  Many  patients 
have  bad  dreams  and  even  delusions,  and,  as  Head  points  out,  the  latter 
are  never  elicited  unless  carefully  inquired  after. 

§  25.  The  chief  complaints — The  chief  complaints  from  which  patients 
with  heart  failure  suffer  are  as  follows  : — • 

Breathlessness. — This  first  appears  on  the  patient  making  some  effort 
which  was  not  previously  attended  with  discomfort,  or  dyspnoea  more  or 


22  DISEASES  OF  THE  HEART 

less  extreme  appears  without  any  apparent  cause.  The  various  forms  of 
respiratory  trouble  are  described  in  Chapter  V. 

The  sense  of  exhaustion. — Many  people  complain  of  feeling  simply 
'  done  up  '.  The  sensation  may  come  on  after  a  bodily  or  mental  effort,  and 
particularly  after  some  excitement.  It  may  be  a  feeling  of  exhaustion  in 
general,  or  it  may  be  located  in  some  definite  region,  as  the  epigastrium,  or 
across  the  chest.  It  is  a  symptom  common  to  trivial  and  transient  condi- 
tions of  heart  exhaustion,  and  to  conditions  of  the  utmost  gravity,  in  the 
latter  case  usually  associated  with  other  phenomena.  A  curious  sense  of 
exhaustion  referred  to  the  legs  in  walking  is  occasionally  complained  of  by 
elderly  people.  They  feel,  after  walking  a  short  distance,  as  if  they  were 
walking  in  water,  or  forcing  the  legs  through  some  viscous  fluid.  A  similar 
condition  is  found  in  patients  suffering  from  heart-block,  and  some  of  these 
are  never  really  comfortable  unless  in  the  recumbent  position. 

Pain  may  appear  in  all  degrees  of  intensity,  and  be  of  slight  or  serious 
import,  the  most  severe  not  necessarily  being  the  most  serious,  nor  the 
slightest  being  of  the  least  significance.  It  may  come  on  with  exertion, 
and  at  once  bring  the  patient  to  a  standstill.  It  may  not  appear  until 
some  hours  after  the  exertion  which  induced  it.  It  may  be  felt  in  various 
regions  of  the  chest,  or  arms,  or  epigastrium,  or  neck.  Its  starting- 
point  and  radiation  should  always  be  noted,  as  it  follows  frequently  very 
definite  lines,  which  reveal  its  true  origin.  A  pain  may  also  be  felt  in  other 
regions,  as  over  the  liver,  when  there  is  enlargement  of  that  organ  due  to 
heart  failure. 

A  sense  of  constriction  or  oppressio7i  of  the  chest  is  a  fairly  common 
accompaniment  of  pain,  but  it  may  appear  independently  of  pain,  and  be 
so  severe  as  to  compel  a  cessation  from  all  effort.  The  symptoms  associated 
with  pain  are  described  in  detail  in  Chapters  VI  and  VII. 

Palpitation  is  the  consciousness  of  the  impact  of  the  heart  against  the 
chest-wall.  The  heart  is  frequently  also  quickened  in  rate,  though  not 
necessarily  so.  In  neurotic  people,  the  hammering  of  the  heart  against  the 
chest-wall  is  most  distressing. 

Consciousness  of  irregular  action  of  the  heart. — Allied  to  this  is  the  con- 
sciousness of  irregularity.  The  most  common  form  of  irregularity  is  that 
where  there  is  an  occasional  long  pause  or  intermission,  the  next  beat  of  the 
heart  being  strong,  giving  rise  to  an  unpleasant  sensation.  So  severe  may 
the  shock  from  this  strong  beat  be  that  in  some  people  it  induces  a  feeling  of 
exhaustion.  Instead  of  being  conscious  of  the  strong  beat  after  the  pause,  the 
patient  may  be  aware  of  the  pause,  and  feel  as  if  the  heart  had  stopped,  or  he 
may  feel  some  curious  sensation  as  a  '  catch  in  his  breath  \     Irregularity 


PRELIMINARY  EXAMINATION  OF  THE  PATIENT  23 

may  give  rise  to  a  slight  fluttering  sensation  in  the  chest.  When  the  heart 
becomes  continually  irregular  for  a  short  or  a  long  period,  this  fluttering 
makes  the  patient  conscious  of  the  abnormal  action  (see  Chapter  XX). 

Haemorrhages. — Rupture  of  an  artery  due  to  high  blood-pressure  acting 
on  a  degenerated  artery  may  give  rise  to  cerebral  apoplexy,  bleeding  under 
the  conjunctiva,  from  the  nose,  &c.  Nose  bleeding  is  not  infrequent  with 
disease  of  the  aortic  valves,  and  in  women  attacks  of  bleeding  from  the  nose 
are  liable  to  occur  at  the  beginning  of  the  menstrual  period.  Haemoptysis 
may  occur  when  the  lungs  are  engorged  or  when  there  is  a  rupture  of  a 
blood-vessel. 

Cerebral  Symptoms 

There  are  a  number  of  symptoms  produced  by  the  brain  dependent  on 
the  inefficiency  of  the  circulation.  I  exclude  from  consideration  here  the 
symptoms  due  to  lesions  of  the  blood-vessels,  as  rupture.  The  symptoms 
induced  more  directly  by  affections  of  the  heart  are  caused  by  a  diminished 
supply  of  blood  reaching  the  brain,  and  the  nature  of  the  symptoms 
depends  on  the  extent  of  that  diminution  and  the  period  during  which  the 
diminished  supply  lasts. 

Dizziness  or  giddiness. — The  first  stage  of  transient  cerebral  anaemia 
is  shown  by  a  sensation  of  giddiness.  It  is  seen  most  characteristically  in 
elderly  people  (particularly  in  tall  people),  when  there  is  arterial  degenera- 
tion. The  attack  usually  comes  on  when  the  individual  makes  a  sudden 
change  in  his  position,  as  in  rising  from  a  couch.  The  attack  may  be  hmited 
to  a  passing  sensation  of  giddiness,  or  the  individual  may  reel  and  stagger 
and  clutch  at  some  object  for  support,  or  he  may  fall.  In  walking,  a  transient 
dizziness  may  come  on  and  the  individual  may  stagger  for  one  or  two 
steps.  The  liability  to  these  attacks  varies  at  different  times — periods  of 
liability  varying  with  periods  when  the  tendency  disappears.  The  attacks 
occurring  in  elderly  people  have  no  special  prognostic  significance,  as  I  have 
known  persons  exhibit  them  over  a  long  period  of  years  and  live  to  over 
eighty  years  of  age.  Exactly  similar  attacks  may  occur  where  the  heart 
fails  to  send  sufficient  blood  into  the  brain,  as  in  paroxysmal  tachycardia, 
where  the  transient  increased  rate  is  accompanied  by  a  diminished  output 
from  the  heart. 

Loss  of  consciousness. — Syncopal  attacks  or  fainting,  when  the  patient 
becomes  limp  and  unconscious,  occur  with  a  diminished  supply  of  blood 
to  the  brain.  This  can  be  brought  about  in  a  variety  of  ways,  and  is 
generally  due  to  an  alteration  in  the  heart's  action.  I  have  made  observa- 
tions and  taken  tracings  of  several  patients  during  syncopal  attacks,  and 


24  DISEASES  OF  THE  HEART 

have  found  a  variety  of  conditions  present.  The  most  common  has  been 
a  slowing  of  the  heart-rate,  with  great  weakness  of  the  pulse,  so  that 
only  a  slight  tracing  was  obtained  by  the  sphygmograph.  In  one  case  the 
heart  was  beating  with  great  rapidity,  but  the  j^ulse  beats  were  small  and 
the  patient  lay  unconscious  for  nearly  half  an  hour.  In  another  case  the 
heart  became  very  slow  in  its  action  and  irregular  with  beats  of  varpng 
strength.  The  more  frequent  forms  of  syncope  are  preceded  by  a  pre- 
liminary sensation  of  extreme  weakness  and  loss  of  sight.  '  All  became 
dark  '  is  a  very  frequent  expression  made  by  the  patient  after  recovery. 

There  is  one  form  of  loss  of  consciousness  which  is  met  with  in  elderly 
people.  The  attacks  come  \vithout  warning  and  are  of  momentary  duration, 
resembUng  "petit  mal.  The  individual  may  be  sitting  at  his  desk,  when  his 
head  suddenly  drops  on  the  desk,  or  he  may  be  standing  or  walking  when 
he  suddenly  falls.  Consciousness  at  once  returns  and  he  is  surprised  to 
find  himself  in  a  strange  posture.  There  is  generally  present  extensive 
arterio-sclerosis  in  these  cases,  with  an  irregular  heart  due  to  extra-systoles. 
I  am  disposed  to  consider  the  attacks  due  to  several  of  these  extra-systoles 
occurring  in  succession,  so  that  there  is  a  temporary  cessation  or  a  diminu- 
tion in  the  amount  of  the  blood  suppljdng  the  brain.  Similar  attacks 
occur  in  the  early  stages  of  heart-block,  but  tracings  of  the  jugular  pulse 
enables  one  to  distinguish  the  condition. 

Adam-Stokes  syndrome. — When  the  blood-supply  of  the  brain  is  com- 
pletely arrested,  loss  of  consciousness  results,  and,  if  prolonged,  epileptiform 
contractions  of  the  muscles  of  the  body  may  result.  The  condition  of 
heart  affection  where  this  is  seen  most  typically  is  in  heart-block — when 
the  auricle  continues  to  beat  at  a  normal  or  quickened  rate  and  the  ventricle 
stands  still  or  beats  at  a  very  slow  rate.  But  identical  cerebral  phenomena 
may  arise  from  other  conditions  when  the  ventricular  contraction  is  too 
slow,  as  in  the  condition  I  describe  under  the  term  '  nodal  bradycardia  ' 
(p.  337),  or  in  the  long  standstill  of  the  whole  heart,  probably  due  to  vagus 
influence,  as  described  by  Laslett  ^°^. 

The  symptoms  due  to  a  diminution  of  the  blood-supply  varies  according 
to  the  degree  of  the  cerebral  anaemia.  Patients  suffering  from  one  of  the 
conditions  just  mentioned  may  show  a  variety  of  symptoms,  as  a  feeling 
of  dizziness,  a  brief  loss  of  consciousness,  or  a  prolonged  loss  of  consciousness 
with  twitchings  of  the  muscles  or  even  convulsions.  These  varying  degrees 
depend  on  the  frequency  of  the  ventricular  systole,  the  milder  phenomena 
being  shown  when  the  ventricular  standstill  is  prolonged,  or  when  the 
contractions  are  at  rare  intervals.  Dr.  O'Connor,  in  the  case  of  nodal 
bradycardia,  described  on  p.  342,  noted  that  his  patient  might  have  twenty 


PRELIMINARY  EXAMINATION  OF  THE  PATIENT  25 

or  thirty  brief  attacks  of  loss  of  consciousness  in  one  day,  and  on  several 
occasions  when  talking  to  his  patient  he  observed  him  suddenly  become 
pale  and  lose  himself  for  a  few  seconds,  the  attack  exactly  resembling  one 
of  petit  mal.  He  has  had  his  finger  on  the  patient's  pulse  on  several  of 
these  occasions  and  felt  it  disappear.  During  longer  pauses  in  the  pulse 
this  patient  had  numerous  epileptic  convulsions. 

Barr  ^^^  has  noted  in  a  case  of  heart-block  that  convulsions  occurred 
when  the  pulse  disappeared  for  twenty  seconds.  In  tracings  taken  from 
the  same  patient,  pauses  of  twenty-one  seconds  and  over  were  followed  by 
convulsions.  With  prolonged  disappearance  of  the  pulse  and  unconscious- 
ness, convulsions  do  not  always  occur,  and  in  the  same  individual  during 
long  pauses  there  may  be  no  convulsions,  or  there  may  be  slight  muscular 
twitchings  or  wide-spread  convulsive  movements,  under  apparently  similar 
circumstances. 

How  long  it  is  possible  for  the  pulse  to  disappear  and  recovery  of  con- 
sciousness to  be  complete  has  not  been  determined  in  the  human  subject, 
nor  can  the  observation  of  the  pulse  alone  be  relied  upon  to  give  informa- 
tion. Leonard  Hill  has  pointed  out  that  the  merest  trickle  of  blood  may 
keep  the  brain  intact,  and  the  fact  that  in  heart-block  the  auricles  are 
beating  may  account  for  a  certain  amount  of  blood  reaching  the  brain. 
That  the  auricle  can  send  blood  into  the  arterial  system  can  be  inferred 
from  the  fact  that  its  contraction  does  affect  the  radial  pulse,  as  shown  by 
Figs.  122-4,  pp.  183-4. 

Hallucinations. — When  the  heart  is  failing  the  blood-supply  of  the 
brain  is  not  fully  maintained  and  certain  symptoms  may  be  detected. 
Thus  the  patient  can  maintain  a  mental  effort  as  in  reading,  or  in  writing, 
only  for  a  short  time,  becoming  easily  fatigued.  The  memory  for  recent 
events  becomes  impaired,  and  what  the  patient  may  read  is  imperfectly 
retained.  In  more  severe  cases  hallucinations  may  appear  and  may  take 
various  forms.  The  patient  may  imagine  that  some  one  is  hiding  behind 
a  door  and  though  in  conversation  admitting  the  unlikelihood  of  such  a 
circumstance,  yet  when  left  alone  the  hallucination  returns  with  a  sensation 
of  terror.  Or  the  patient  may  wake  up  and  imagine  he  sees  objects,  as  an 
arm  projecting  from  the  ceiling,  or  the  sound  of  some  one  on  the  stair, 
or  of  soldiers  marching  past  in  the  street.  Head  ^^  has  dealt  very  fully  with 
this  matter,  and  points  out  that  the  patient  usually  conceals  these  hallucina- 
tions until  he  is  directly  questioned  concerning  them. 


CHAPTER  V 

Respiratory  Symptoms 

§  26.  Breathlessness,  or  aii-  hunger. 

27.  The  sense  of  suffocation. 

28.  Inability  to  stop  breathing. 

29.  Quiet,  rapid  breathing,  free  from  distress. 

30.  Continuous  laboured  breathing. 

31.  Laboured  breathing  brought  on  by  exertion. 

32.  Attacks  of  breathlessness  (cardiac  asthma). 

33.  Cheyne-Stokes  respiration. 

34.  Slow  respiration. 

35.  Pulmonary  haemorrhage. 

36.  Acute  suffocative  oedema  of  the  lungs. 

The  respiratory  symptoras  arising  in  the  course  of  heart  affections  are 
so  numerous,  and  the  conditions  causing  them  so  multifarious,  that  it  is 
impossible  to  deal  exhaustively  with  this  subject.  The  factors  concerned 
in  the  production  of  any  one  of  the  forms  of  respiratory  trouble  are  often 
difficult  to  recognize,  and  I  shall  not  attempt  any  strict  analysis  of  these 
factors,  but  limit  myself  to  the  more  apparent  clinical  forms  that  accompany 
heart  affections. 

§  26.  Breathlessness,  or  air  hunger — There  is  normally  a  '  desire  to 
breathe  ',  and  under  certain  circumstances  this  may  be  intensified  so  that 
there  is  a  '  hunger  '  for  air.  The  sense  of  air  hunger  compels  laboured 
breathing  so  that  the  term  '  breathlessness  '  includes  the  subjective  sensation 
and  the  objective  symptom.  The  centre  for  respiration  in  the  medulla  is 
influenced  by  its  blood-supply,  and  its  nervous  connexion  with  the  peri- 
phery. A  free  blood-supply  is  necessary  to  supply  oxygen  and  remove  the 
carbonic  acid,  and  an  insufficient  interchange  of  these  gases  is  betrayed  by 
an  increased  activity  of  the  centre,  thus  giving  rise  to  breathlessness.  The 
respiratory  centre  is  also  receptive  to  peripheral  stimulation,  as  from  sensory 
nerves  of  the  skin  and  from  cardiac  and  pulmonary  nerves. 

An  absence  of  the  sense  to  respire  may  occur  for  a  short  period  as  in  the 
apnoeic  stage  of  Cheyne-Stokes  respiration.  John  Hunter  ^'^'^  gives  a  curious 
account  of  an  attack  from  which  he  suffered,  when  he  lay  pulseless  but 
conscious  ;  observing  he  did  not  breathe,  and  had  no  desire  to  do  so, 
he  thought  he  must  die  if  he  did  not  breathe,  and   by  an  effort   of  will 


RESPIRATORY  SYMPTOMS  27 

continued  to  breathe  until  his  pulse  returned  and  the  automatic  respiration 
was  established. 

§  27.  The  sense  of  suffocation.— This  is  difficult  to  describe,  and  is 
referred  usually  to  the  upper  part  of  the  chest  and  throat.  The  mechanism 
is  obscure.  It  is  a  frequent  accompaniment  of  heart  affections,  from 
temporary  weakness  of  the  heart  to  the  gravest  forms  of  heart  disease,  and 
its  significance  may  be  slight,  or  in  serious  heart  trouble  it  may  be  a  very 
grave  sign. 

§  28.  Inability  to  stop  breathing — I  have  been  struck  by  the  fact 
that  while  taking  tracings  of  the  jugular  and  other  pulses  many  patients 
are  unable  to  stop  breathing.  When  asked  to  hold  their  breath,  they  will 
shut  their  mouths,  but  are  unable  to  stop  breathing  through  the  nose.  If 
the  nose  be  pinched,  they  then  complain  of  distress  (air  hunger).  This 
condition  only  arises  in  extreme  heart  failm-e,  and  as  the  heart  regains 
strength  we  may  recognize  the  fact  by  the  abihty  to  hold  the  breath. 

§  29.  Quiet,  rapid  breathing,  free  from  distress — In  many  cases  of 
heart  failure,  when  the  patient  is  lying  quiet,  no  definite  symptom  can  be 
found  save  that  of  a  respiration  more  rapid  than  normal.  There  is  no 
distress,  and  the  symptom  is  apt  to  be  overlooked.  Sometimes  I  have 
failed  to  recognize  it  until  I  have  come  to  analyse  tracings  where  the 
respiratory  movements  had  been  taken.  Where,  as  sometimes  happens, 
a  patient  describes  certain  feehngs  (as  angina  pectoris)  which  we  are  bound 
to  recognize  as  cardiac  in  origin,  but  where  physical  examination  reveals 
no  sign  of  mischief,  the  recognition  of  more  rapid  respiration  may  prevent 
us  from  vicA^ing  too  hghtly  the  condition  of  the  patient.  This  symptom 
is  of  the  greatest  importance  in  patients  suffering  from  affections  of  the  heart, 
particularly  in  mitral-stenosis,  in  exhausting  diseases  like  typhoid  fever, 
and  in  all  conditions  that  compel  the  weakly,  and  particularly  the  elderly, 
to  lie  on  their  backs,  as  e.  g.  when  suffering  from  a  broken  leg.  In  such 
cases  the  lying  in  bed,  while  favouring  the  work  of  the  left  ventricle,  embar- 
rasses the  work  of  the  right  by  restricting  the  respiratory  movement.  As 
a  result  of  this  restraint  of  the  ribs,  the  breathing  becomes  shallow.  The 
effect  is  to  retard  the  flow  of  blood  through  the  less  mobile  part  of  the  lungs, 
and  in  consequence  stasis  at  the  base  of  the  lungs  results  (see  §  190). 

§  30.  Continuous  laboured  breathing — This  occurs  characteristically, 
at  the  beginning  of  what  is  called  '  sudden  failure  of  compensation  '.  The 
patient  cannot  lie  down,  but  sits  up  breathing  in  short  quick  gasps.  The 
slightest  exertion,  such  as  is  entailed  by  changing  to  a  more  comfortable 
position,  immediately  aggravates  the  distress.  This  form  of  breathing  is 
best  seen  in  cases  of  dilatation  of  the  heart  with  a  rapid  irregular  pulse, 


28  DISEASES  OF  THE  HEART 

and,  in  fact,  the  whole  respiratory  distress  is  often  the  outcome  of  the 
heart  taking  on  the  nodal  rhythm  which  is  manifested  by  the  irregularity 
(Chapter  XX).  With  slowing  of  the  heart's  action  and  other  evidences 
of  cardiac  improvement,  the  respiratory  distress  gradually  disappears,  but 
is  liable  at  first  to  be  brought  on  readily  by  a  slight  exertion. 

§  31.  Laboured  breathing  brought  on  by  exertion — This  is  a  symp- 
tom common  to  a  great  many  affections  besides  heart  troubles,  but  its  asso- 
ciation with  a  weak  heart  is  so  common  that  it  should  at  all  times  lead  to 
an  inquiry  as  to  the  condition  of  the  heart.  It  may  occur  with  every  form 
of  heart  affection.  It  is  of  very  great  use  in  estimating  the  strength  of  the 
heart,  as  its  appearance  indicates  in  a  rough  way  the  degree  of  exhaustion. 
The  earlier  it  appears,  the  less  the  reserve  power  of  the  heart.  On  the  other 
hand,  improvement  may  be  indicated  by  the  gradual  return  of  the  ability 
of  the  patient  to  undertake  with  comfort  greater  exertion.  The  forms  of 
exertion  that  induce  it  are  very  puzzling.  Some  patients  can  lift  great 
weights,  and  pursue  the  hard  work  associated  with  their  calling,  yet  cannot 
walk  up  a  slight  hill  without  complaining  of  being  short-winded  ;  or  they 
suffer  in  the  same  way  on  going  into  the  cold  air.  Some  can  cycle  in  comfort, 
while  others  cannot  cycle,  but  can  walk  with  comfort  on  the  level.  I  cannot 
explain  these,  and  other  peculiarities,  but  note  them  as  clinical  facts. 

§  32.  Attacks  of  breathlessness  (cardiac  asthma) — A  form  of 
respiratory  distress  which  comes  on  usually  in  the  night,  sometimes  suddenly 
arousing  the  patient  from  sleep,  has  received  the  name  of  '  Cardiac  Asthma  '. 
An  attack  of  this  sort  is  sometimes  the  first  serious  sign  of  heart  trouble, 
though  on  inquiry  an  account  can  usually  be  obtained  of  a  period  prior  to 
the  attack  when  there  was  a  distinct  hmitation  of  the  field  of  cardiac  response. 
The  patient  may  have  gone  to  bed  in  his  usual  health  and  according  to  his 
usual  custom,  and  after  three  or  four  hours'  sleep  he  is  awakened  with  a 
feeling  of  suffocation,  and  an  intense  desire  to  breathe  deeply.  He  sits  up 
in  bed,  and  breathes  in  deep  and  laboured  fashion,  A  sense  of  great  pros- 
tration may  add  to  his  suffering.  Wheezing  sounds  may  appear  in  the 
chest,  and  he  may  cough  up  some  frothy  phlegm.  The  attack  may  last 
for  half  an  hour  or  longer  ;  then  the  breathing  becomes  quieter,  and  he 
is  able  to  lie  down,  though  he  keeps  starting  up,  and  finally  assumes  a  position 
with  his  head  and  shoulders  raised,  passing  the  remainder  of  the  night  in 
uneasy  slumber.  Once  these  attacks  begin  they  are  apt  to  continue,  and 
the  nights  of  the  patient  often  become  periods  of  great  distress.  The  fear 
of  the  attack  may  keep  the  patient  awake,  and  should  he  drop  off  to  sleep 
he  awakes  with  a  start  at  the  first  sign  of  embarrassed  breathing. 

The  class  of  case  which  shows  this  condition  most  characteristically 


RESPIRATORY  SYMPTOMS  29 

is  the  elderly,  and  those  who  suffer  from  cardio-sclerosis.  Generally  they 
have  a  high  blood-pressure,  and  the  heart  is  usually  regular  except  for  the 
presence  of  occasional  or  frequent  extra-systoles.  In  these  cases  we  some- 
times find  the  best  examples  of  the  pulsus  alternans.  The  cause  of  this 
form  of  asthma  is  not  quite  clear.  I  have  found  the  great  distress  induced 
by  this  condition  in  many  cases  insusceptible  to  treatment,  but  lately 
I  have  been  giving  massive  doses  of  oxygen,  in  some  cases  with  very  gratify- 
ing success  (see  p.  278). 

§  S3-  Cheyne-Stokes  respiration — In  all  cases  of  heart  affection 
where  there  is  reason  to  suspect  cardio-sclerosis,  or  where  there  is  a  high 
blood-pressure  from  such  causes  as  arterio-sclerosis  and  Bright's  disease, 
and  where  we  get  a  history  of  breathlessness,  quiet  observation  should  be 
made  when  the  patient  is  perfectly  still,  and  nothing  attracting  his  attention. 
Under  such  circumstances,  the  patient's  breathing  may  occasionally  be  found 
to  take  on  a  peculiar  rhythmical  character.  Instruction  should  also  be 
given  for  the  attendants  to  note  the  character  of  respiration  during  sleep. 

The  character  of  the  breathing  is  a  rhythmical  variation  in  the  size 
of  the  respiratory  movements — a  gradual  passage  from  a  state  of 
complete  or  almost  complete  cessation  to  a  condition  of  breathing  where 
the  respiratory  movements  are  deep  and  laboured  (see  Figs.  4  and  5, 
Plate  I).  When  the  breathing  gradually  slows  and  ultimately  stops,  the 
patient's  mental  condition  frequently  becomes  a  blank,  and  is  accompanied 
usually  by  twitching  of  some  muscles,  especially  to  be  noticed  in  those  of 
the  hand  and  arm.  With  the  resumption  of  the  breathing,  he  wakes,  and 
may  resume  a  conversation  that  he  had  been  pursuing  before  the  slowing 
of  the  breathing  set  in. 

Usually  no  material  change  can  be  detected  in  the  action  of  the  heart 
during  the  diverse  phases  of  respiration.  Sometimes,  however,  certain 
changes  may  appear  in  the  pulse  coincident  with  the  respiratory  phases. 
One  patient  with  a  sclerotic  heart  (Case  23,  Appendix  V)  had  shown 
a  weU-marked  pulsus  alternans  for  many  months  (Fig.  249),  and  towards 
the  end  of  his  life  he  developed  Cheyne-Stokes  respiration  (Fig.  6,  Plate  I). 
During  the  respiratory  phases  there  was  a  distinct  increase  in  this  form  of 
irregularity  in  the  radial  pulse.  I  took  his  blood-pressure  during  a  period 
of  Cheyne-Stokes  respiration,  and  found  that  it  fell  5  to  10  mm.  Hg.  during 
the  apnoeic  stage.  This  variation  can  be  made  out  in  the  pulse  tracing  in 
Fig.  6,  Plate  I,  where  it  shows  a  greater  amplitude  of  beat,  and  lowering  of 
the  base  line  during  the  fall  of  blood-pressure,  i.  e.  during  the  apnoeic  period. 
Gibson  has  also  described  a  fall  of  blood-pressure  during  the  apnoeic  stage. 
In  Fig.  7,  Plate  I,  there  is  a  tracing  from  a  patient  who  had  hiccough  as  well 


30  DISEASES  OF  THE  HEART 

as  Cheyne-Stokes  respiration,  and  Cushny^^^,  commenting  on  this  case  before 
the  Physiological  Society,  remarked,  '  During  the  intervals  of  apnoea,  the 
rhythm  of  the  hiccough  was  more  rapid  than  during  the  periods  of  active 
respiration,  but  the  violence  of  the  spasms  seemed  somewhat  less. 

'  The  physiology  of  hiccough  is  still  obscure,  and  we  are  not  aware  of  any 
record  of  the  movements  having  been  taken  previously.  It  is  generally 
stated  to  be  a  reflex  movement  of  the  diaphragm,  originating  from  some 
abnormal  irritation  of  the  stomach.  If  the  respiratory  centre  is  involved 
in  the  reflex,  as  is  generally  held,  it  must  have  remained  excitable  by  nervous 
impulses  in  this  case  when  the  normal  chemical  stimulus  failed  to  induce 
respiration.  The  slowing  of  the  hiccough  rhythm  during  the  periods  of 
active  respiration  is  striking,  and  may  perhaps  be  analogous  to  the  inter- 
ference of  two  reflexes  with  a  final  common  path  (Sherrington)  ;  here  only 
one  afferent  stimulus  is  of  nervous  origin,  however,  the  other  being 
chemical.' 

Usually  the  patient  is  unaware  of  the  occurrence  of  this  periodic  respira- 
tion, and  it  causes  him  no  distress.  On  the  other  hand,  it  may  occasion 
acute  distress  :  the  patient  may  drop  off  to  sleep,  and  this  form  of  respiration 
gradually  appears,  and  during  the  apnoeic  stage  the  patient  awakes  with 
a  most  distressful  sensation  of  suffocation.  So  terrible  is  this  that  patients 
extremely  exhausted  may  spring  suddenly  out  of  bed  in  an  extremity  of 
terror. 

The  great  majority  of  cases  of  Cheyne-Stokes  respiration  are  brought 
on  by,  or  associated  with,  cardio-sclerosis,  arterial  disease,  and  high  blood- 
pressure.  It  disappears  with  the  sudden  fall  of  blood-pressure  due  to 
dilatation  of  the  heart.  It  may  be  made  temporarily  to  disappear  by 
massive  doses  of  oxygen  ;  or  on  the  inhalation  of  small  quantities  of  COo 
(Pembery  *^'').  Haldane  and  Poulton*^"  have  produced  the  condition 
by  forced  breathing,  and  conclude  that  the  periodic  breathing  is  due  to 
the  '  disappearance  of  the  (indirect)  excitatory  effects  of  want  of  oxygen 
in  the  respiratory  centre  '. 

In  the  great  majority  of  cases  of  arterio-sclerosis  and  Bright 's  disease 
it  is  usually  the  beginning  of  the  end,  the  patients  dying  within  a  few  months 
or  weeks,  or  even  a  few  days  of  its  onset.  In  a  few  cases  I  have  seen  it  appear 
two  or  three  years  before  death.  It  calls  for  no  special  treatment  save 
when  the  apnoeic  stage  produces  the  terrible  sense  of  suffocation  ;  then 
morphia  or  chloral  generally  relieves  this  feature  without  altering  the 
respiration. 

Cheyne-Stokes  respiration  must  be  kept  distinct  from  certain  other 
forms    of    periodic    respiration.      Hibernating    animals    show    a    form    of 


RESPIRATORY  SYMPTOMS  31 

periodic  respiration,  also  some  children  during  sleep.  It  appears  also  in 
some  cases  of  tubercular  meningitis. 

Loss  of  consciousness  does  not  always  ensue  during  the  apnoeic  stage 
of  Cheyne-Stokes  respiration,  as  shown  by  the  following  instance.  I  saw  in 
consultation  a  clergyman,  aged  fifty,  who  had  a  paralytic  seizure  two  years 
previously,  resulting  in  an  ordinary  hemiplegia.  When  I  saw  him  he  was 
lying  in  bed  quite  conscious,  extremely  prostrate,  with  a  pulse  rate  of  180 
per  minute,  with  t3rpical  periodic  respiration.  During  the  apnoeic  stage 
he  was  quite  conscious,  and  could  talk  intelhgently,  his  voice  was  faint  and 
reedy  in  quality,  diminishing  in  loudness  towards  the  end  of  his  remarks. 
His  medical  attendant  told  me  he  had  suffered  off  and  on  from  this  condition 
for  three  years.  This  case  corresponds  to  a  description  given  by  John 
Hunter  ^^,  who  says,  '  A  gentleman  had  a  singular  asthmatic  affection,  and 
his  breathing  gradually  stopped  and  again  gradually  recurred,  but  became 
violent,  and  thus  constantly  and  alternately  held  two  or  three  minutes, 
and  when  the  breatliing  ceased  yet  he  spoke  although  but  faintly.' 

§  34.  Slow  respiration — There  is  a  number  of  individuals  in  whom 
the  respirations  during  rest  are  much  slower  than  normal,  7  to  10  per  minute. 
The  slow  respiration  induces  an  irregular  action  of  the  heart,  and  is  described 
in  Chapter  VIII.  The  condition  is  probably  due  to  vagus  stimulation, 
and  I  have  been  able  to  produce  it  artificially  by  the  administration  of 
digitalis. 

§  35.  Pulmonary  haemorrhage — Bleeding  from  the  lungs  is  not  an 
infrequent  complication  in  heart  failure.  It  is  most  commonly  seen  in  the 
terminal  stages  of  arterio-sclerosis,  with  the  fall  of  blood-pressure  that 
indicates  dilatation  of  the  heart  and  stasis  of  blood  in  the  lungs.  In  these 
cases  the  expectoration  is  either  blood-stained  or  it  is  almost  entirely 
composed  of  lumps  of  dark  clotted  blood.  Post  mortem  there  are  usually 
found  several  hard  patches  of  ecchymosed  blood  at  the  base  of  the  lungs. 
In  the  young  with  mitral  stenosis,  profuse  haemoptysis  may  occur,  and  is 
generally  a  sign  of  extreme  gravity. 

In  other  forms  of  heart  affection,  haemorrhage  more  or  less  free  may 
occur,  and  give  the  patient  considerable  relief,  and  be  followed  by  no  serious 
consequence.  In  fact,  if  we  find  the  patient  on  the  whole  with  a  fair  amount 
of  reserve  force,  whatever  the  nature  of  the  heart  lesion,  there  need  be  no 
immediate  alarm  from  a  free  haemoptysis  when  due  to  cardiac  trouble. 

A  serious  form  of  haemoptysis  arises  from  a  pulmonary  infarct,  or  a  pul- 
monary apoplexy  ;  in  these  cases  the  symptoms  are  extremely  varied  in 
severity.  Thus  I  have  seen  patients  with  phlebitis  of  the  veins  of  the  leg, 
or  after  confinement,  die  in  a  few  minutes  with  symptoms  of  great  respiratory 


32  DISEASES  OF  THE  HEART 

distress.  In  some  cases  I  have  seen  the  most  intense  dyspnoea  with  gradual 
loss  of  consciousness  go  on  for  four  or  five  hours,  and  then  suddenly  the 
dyspnoea  ceases  and  the  consciousness  returns.  After  twelve  hours  the 
patient  has  expectorated  large  quantities  of  pink-stained  jelly-Uke  mucus. 
I  have  also  seen  cases  of  pulmonary  infarct,  as  after  a  fracture  of  the  tibia, 
where  the  only  evidence  was  the  expectoration,  for  three  or  four  days,  of 
dark-coloured  blood,  in  small  quantities  at  a  time,  followed  by  complete 
recovery.  Presumably  the  difference  in  the  symptoms  in  these  cases 
depended  on  the  size  of  the  infarct  or  the  extent  of  the  apoplexy. 

§  ^6.  Acute  suffocative  oedema  of  the  lungs A  peculiar  form  of 

oedema,  of  which  I  have  only  seen  a  few  cases,  is  that  in  which  the  patient 
is  suddenly  seized  with  breathlessness,  usually  during  the  night,  followed 
speedily  by  the  welling  out  of  the  mouth  and  nose  of  large  quantities  of 
froth.  Usually  the  patient  succumbs  within  an  hour  of  the  commencement 
of  the  attack.  The  conditions  giving  rise  to  it  are  obscure,  and  it  occurs 
in  a  great  variety  of  cases.  An  excellent  account  of  a  case,  and  the  literature 
on  this  subject,  are  given  by  L.  Williams  ^°. 


CHAPTER  VI 

Reflex,  or  Protective  Phenomena 

§  37.    Classification  of  symptoms  in  visceral  disease. 

38.  Insensitiveness  of  the  viscera  to  ordinary  stimuli. 

39.  The  mechanism  by  which  pain  and  other  reflex  phenomena  are  produced  in  visceral 

disease  (the  viscero-sensory  reflex). 

40.  The  purpose  of  visceral  reflexes. 

41.  Why  pain  is  referred  to  regions  remote  from  the  organ. 

42.  The  relationship  of  the  heart  to  sensory  nerves. 

43.  The  viscero-motor  reflex. 

44.  Vagal  sensory  reflex. 

45.  Conditions  in  which  angina  pectoris  js  induced. 

46.  Conditions  giving  rise  to  attacks  of  angina  pectoris. 

47.  Association  of  angina  pectoris  with  exhaustion  of  the  muscle  of  the  heart. 

48.  Association  of  angina  pectoris  with  impairment  of  the  function  of  contractility. 

49.  Summation  of  stimuli  as  a  cause  of  angina  pectoris. 

§  37.  Classification  of  symptoms  in  visceral  disease When  the 

symptoms  of  visceral  disease  are  carefully  analysed  there  appears  a  great 
similarity  in  the  nature  and  origin  of  certain  of  them,  which  permits  of  their 
division  into  three  groups  ; — first,  symptoms  due  to  changes  in  the  organ 
itself — in  the  case  of  the  circulatory  system,  changes  in  the  movements 
of  the  heart  and  blood-vessels  ;  second,  symptoms  observed  in  remote 
organs  and  tissues  which  suffer  indirectly  from  the  primary  lesion,  for 
instance,  jaundiced  skin  in  liver  affections,  uraemic  convulsions  in  renal 
disease  and  dropsy,  oedema  or  albuminuria  in  heart  failure  ;  third,  reflex 
or  protective  phenomena,  which  form  the  subject  of  this  chapter. 

While  the  character  of  the  symptoms  in  the  first  two  divisions  depends 
on  the  size  and  specific  function  of  each  organ,  the  reflex  phenomena  pro- 
duced by  all  organs  have  a  great  resemblance.  This  is  particularly  the  case 
with  all  the  hollow  muscular  organs.  They  have  similar  origins  and  their 
reflexes  are  similar  in  character,  and  are  only  modified  by  the  special  develop- 
ment of  each.  In  spite  of  the  seeming  dissimilarity  in  the  form  and  function 
of  the  digestive  tube,  uterus,  ureter,  and  heart,  they  are  fundamentally 
the  same,  and  the  reflexes  associated  with  them  are  of  a  like  nature.  Hence 
the  nature  of  obscure  symptoms  in  affections  of  the  heart  may  be  revealed 
by  an  inquiry  into  the  meaning  of  similar  phenomena  presented  by  these 
organs,  which  have  at  first  sight  so  little  affinity  with  it. 

MACKENZIE  J) 


34  DISEASES  OF  THE  HEART 

§  38.  Insensitiveness  of  the  viscera  to  ordinary  stimuli In  order 

to  appreciate  the  reflex  symptoms  in  visceral  disease  we  must  keep  in  mind 
the  functions  of  the  nerves  that  supply  them. 

The  nerve-supply  of  the  body  is  included  in  the  two  great  systems,  the 
autonomic  and  the  cerebro-spinal.  The  autonomic  includes  the  whole  of 
the  sympathetic  nerves,  and  certain  cerebral  nerves,  of  which  the  vagus 
is  the  only  one  that  concerns  us  here. 

The  tissues  and  organs  supplied  by  the  nerves  from  the  autonomic 
system  are  not  endowed  with  sensation  in  the  sense  in  which  the  term  is  used 
in  regard  to  tissues  supplied  by  the  cerebro-spinal  nerves.  The  skin,  muscle, 
and  other  tissues  of  the  external  body-wall  are  readily  sensitive  to  all  forms 
of  stimuli  that  produce  such  sensations  as  touch,  pain,  heat,  and  cold,  whereas 
the  viscera  supplied  only  by  the  autonomic  system  are  totally  irresponsive 
to  such  stimuli.  Thus  such  organs  as  the  heart,  stomach,  bowels,  liver, 
kidney,  can  be  cut,  torn,  burnt,  and  no  sensation  elicited.  Yet,  as  we  know, 
pain  of  a  most  excruciating  character  can  arise  from  visceral  affections. 
Harvey  ^^  describes  how  he  touched  the  exposed  heart  of  the  son  of  Viscount 
Montgomery  and  found  it  without  sensation.  Surgeons  in  pre-chloroform 
days  incidentally  refer  to  the  insensitiveness  of  the  viscera.  Thus  Richerand  ** 
describes  how,  in  operating  in  the  neighbourhood  of  the  heart,  he  found  the 
pericardium  insensitive,  and  I  have  repeatedly  verified  this  observation  in 
cases  where  the  ribs  have  been  resected.  The  following  experience  illustrates 
the  insensitiveness  of  the  viscera,  and  at  the  same  time  affords  an  insight 
into  the  manner  in  which  visceral  pain  arises. 

I  had  occasion  to  resect  the  bowel  in  a  conscious  subject  under  the 
following  circumstances.  He  had  an  umbilical  hernia,  and  had  worn  for 
years  a  pad  tightly  pressed  over  it,  until  the  skin  had  ulcerated.  The 
ulceration  had  finally  penetrated  into  the  bowel,  and  his  food  was  dis- 
charged through  the  fistula.  It  was  resolved  to  resect  the  bowel,  but  the 
patient  would  not  be  anaesthetized.  Observing  that  the  skin  was  already 
ulcerated,  and  that  the  tissues  forming  the  external  wall  were  not  very 
sensitive,  so  that  the  abdominal  cavity  could  be  opened  with  Uttle  pain, 
I  reasoned  that  the  after-operation  could  be  performed  painlessly.  It  turned 
out  as  I  had  expected,  and  I  was  able  to  break  down  numerous  old  and 
recent  peritoneal  adhesions,  to  detach  them  from  the  liver  and  bowel,  to 
resect  a  piece  of  bowel  and  mesentery,  and  to  stitch  these  structures  without 
the  patient  experiencing  the  slightest  sensation.  But  I  found  that  he 
occasionally  groaned  with  pain  when  I  was  not  touching  him,  and  watching 
to  see  the  cause  I  found  that  the  upper  part  of  the  resected  bowel,  which  was 
laid  on  one  side  in  a  warm  aseptic  cloth,  occasionally  passed  into  peristalsis, 


REFLEX,  OR  PROTECTIVE  PHENOMENA  35 

contracting  from  a  wide  tube  to  a  thick  fleshy  rod  ;  when  this  happened  the 
patient  groaned  with  pain.  I  asked  him  where  he  felt  the  pain,  and  he 
passed  his  hand  invariably  over  the  umbilical  region.  I  started  the  peri- 
stalsis several  times  by  slightly  pinching  the  bowel,  and  each  time  the  patient 
felt  the  pain.  Here  before  my  eyes  was  the  cause  of  the  pain,  and  the  seat 
of  origin  of  the  pain  was  at  least  twelve  inches  away  from  the  part  in  which 
the  pain  was  felt. 

From  this  experience  the  following  deductions  can  be  made  :  first, 
that  the  stimuli  that  produce  pain  and  other  sensations  in  the  external 
body-wall  are  not  adequate  to  produce  these  sensations  when  applied  to  the 
viscera  ;  second,  that  violent  contraction  of  non-striped  muscular  fibres 
can  produce  pain,  but  the  region  in  which  the  pain  is  felt  is  different  from 
that  in  which  the  contracting  muscle  lies. 

This  isolated  experience  has  been  confirmed  by  many  other  observations 
I  have  made,  and  in  part  confirms  the  experiments  made  by  Haller^"  more 
than  150  years  ago  upon  animals,  when  he  showed  that  they  were  indifferent 
to  severe  mutilation  of  their  viscera,  so  long  as  the  external  body-wall  was 
not  interfered  with. 

These  experiences  compel  one  to  look  for  an  explanation  of  the  production 
of  visceral  pain  other  than  that  which  suffices  to  explain  its  production  from 
the  stimulation  of  the  external  body-wall,  and  the  following  explanation 
seems  satisfactorily  to  account  for  the  matter,  and  to  explain  the  peculiar 
nature  of  the  sensory  phenomena  that  arise  in  visceral  disease. 

§  39.  The  mechanism  by  which  pain  and  other  reflex  phenomena 
are  produced  in  visceral  disease  (the  viscero-sensory  reflex)  — When 
a  nerve  that  terminates  in  a  sense  organ  is  stimulated  in  any  part  of  its 
course  from  the  periphery  to  the  brain,  a  stimulus  is  conveyed  to  the  brain 
of  a  kind  similar  to  that  induced  when  the  peripheral  end-organ  is  stimulated. 
Thus  the  stimulation  of  any  part  of  the  optic  nerve  or  auditory  nerve  gives 
rise  to  the  sensation  of  light  or  of  sound.  In  the  same  manner,  if  a  sensory 
nerve  be  stimulated  in  any  part  of  its  course  through  the  brain,  spinal  cord, 
or  trunk  of  the  nerve,  the  resultant  sensation  is  referred  to  the  peripheral 
distribution  of  the  nerve  in  the  external  body-wall. 

Fig.  8  is  a  diagram  representing  the  brain  and  spinal  cord  (S.C.)  with 

a  sensory  nerve  (S.N.)  passing  from  the  skin  (Sk)  through  the  spinal  cord 

to  the  brain.     A  stimulus  applied  to  the  skin,  or  to  the  sensory  nerve 

between  the  skin  and  the  cord,  or  to  the  sensory  nerve  in  the  cord,  gives 

rise  to  a  sensation  referred  by  the  brain  to  the  portion  of  skin  innervated 

by  the  nerve,  though  the  stimulus  may  have  affected  the  nerve  after  it  had 

left  the  skin.     In  the  diagram,  a  viscus  (H)  is  represented,  and  its  nerve 

D  2 


36 


DISEASES  OF  THE  HEART 


(Sy.  N.)  is  seen  passing  to  the  spinal  cord.     In  the  normal  processes  of  life, 
a  stream  of  energy  from  the  viscera  is  continually  passing  by  the  afferent 


Fig.  8.  Diagram  sho^-ing  the  mechanism  producing  visceral  pain.  From  the  viscus  H  an 
abnormal  stimulus  is  conveyed  by  the  sympathetic  nerve  (Sy.  N.)  to  the  spinal  cord  S.C.  On 
reaching  the  cord  the  abnormal  stimulus  spreads  beyond  the  sympathetic  centre  and  affects 
nerve-cells  in  its  immediate  neighbourhood.  The  cells  so  stimulated  react  according  to  their 
function,  the  sensory  causing  a  sensation  which  the  brain  recognizes  as  pain,  and  refers  to  the 
peripheral  distribution  of  the  sensory  nerve  (S.N.)  in  the  skin  (Sk)  or  muscle  (31),  the  motor 
(M.N.)  producing  contraction  of  the  muscle  (31).  The  abnormal  stimulation  may  leave  a 
portion  of  the  cord  abnormally  irritable  (shaded  portion),  so  that  the  tissues  supplied  by 
nerves  from  that  portion  of  the  cord  are  hyperalgesic,  and  attacks  of  pain,  as  of  angina  pectoris, 
are  more  easily  provoked. 


nerves  to  the  spinal  cord,  and  continuously  playing  upon  the  efferent  nerves 
that  run  to  muscles,   blood-vessels,   and   so  forth.     These  processes  are 


REFLEX  OR  PROTECTIVE  PHENOMENA  37 

conducted  so  that  they  give  rise  to  no  appreciable  sensation.  If,  however, 
a  morbid  process  in  a  viscus  gives  rise  to  an  increased  stimulation  of  the  nerves 
passing  from  the  viscus  to  the  spinal  cord,  this  increased  stimulation  affects 
neighbouring  centres.  If  it  excites  the  sensory  nerve  represented  in  the 
diagram  as  passing  from  the  skin  to  the  brain,  the  resulting  sensation  will 
be  referred  by  the  brain,  not  to  the  viscus,  but  to  the  peripheral  distribution 
of  the  sensory  nerve.  Thus  it  was  that  when,  in  the  course  of  the  operation 
which  I  have  described,  the  bowel  contracted,  the  resulting  pain  was  referred 
not  to  the  bowel,  but  to  the  peripheral  distribution  of  the  sensory  nerves 
in  the  region  of  the  umbiHcus — thus  the  pain  in  visceral  disease  is  seen  to 
be  of  a  reflex  character — a  viscerosensory  reflex. 

In  the  diagram  there  is  shown  a  motor  nerve  {M.N.)  arising  in  the  cord 
and  passing  to  a  muscle  {M).  The  stimulus  from  the  viscus  [H)  passing 
into  the  spinal  cord,  may  excite  the  cells  of  origin  of  the  motor  nerves,  with 
the  result  that  the  muscle  is  stimulated  to  contract  ;  hence  we  get  the 
viscero-motor  reflex.  This  reflex  is  best  seen  in  affections  of  the  abdominal 
viscera  when  the  abdominal  wall  becomes  hard,  due  to  tonic  contraction 
of  the  muscles. 

When  a  portion  of  the  spinal  cord  becomes  violently  stimulated  by  reason 
of  a  visceral  affection,  that  portion  of  the  cord  may  remain  for  a  lengthened 
period  in  an  over-excitable  state,  so  that  all  the  nerves  that  arise  from  this 
portion  of  the  cord  may  be  much  more  easily  stimulated.  This  can  be 
demonstrated  in  many  cases  of  visceral  disease  by  the  hyperalgesic  state 
of  portions  of  the  external  body-wall,  and  by  the  exaggerated  motor  reflexes. 
In  such  instances,  stimulation  of  the  skin  or  muscles,  as  by  light  pinching 
between  finger  and  thumb  of  such  weak  force  that  normally  it  would  only 
result  in  the  sensation  of  touch,  is  felt  by  the  patient  as  pain.  Light  stroking 
of  the  skin  with  a  pin  head  may  be  felt  as  pain,  and  produces  very  readily 
a  strong  reflex  contraction  of  the  muscles  whose  nerves  arise  from  the  same 
portion  of  the  cord.  A  further  result  of  this  irritable  focus  in  the  cord  is 
that  the  visceral  stimulation  more  readily  induces  pain,  and  not  only  may 
the  original  attacks  of  pain  (as  in  angina  pectoris,  renal  and  bihary  colic)  be 
more  easily  induced,  but  stimuli  from  other  sources  may  induce  the  attack 
of  pain.  Thus  in  cases  of  gall-stones  with  hyperalgesia  of  the  external 
body-wall  over  the  region  of  the  liver,  the  ingestion  of  the  food  into  the 
stomach  may  give  rise  to  much  pain  in  the  hjrperalgesic  tissues. 

§  40.  The  purpose  of  visceral  reflexes Reflexes  have  been  studied 

with  the  greatest  minuteness,  and  the  work  of  Sherrington  *^  demonstrates 
the  extraordinary  variety  and  complexity  of  the  spinal  reflexes,  but  their 
purpose  has  been  to  a  great  extent  overlooked.     The  main  purpose  of  many 


38  DISEASES  OF  THE  HEART 

reflexes  has  been  either  to  remove  the  body  from  the  reach  of  injurious 
influences,  or  to  interpose  a  firmly  contracted  muscle  between  the  agent 
threatening  the  injury  and  the  organ.  It  may  even  be  true,  as  Herbert 
Spencer  suggests,  that  the  evolution  of  muscles  and  the  segmentation  of 
the  body  was  due  to  the  necessity  of  protection  when  the  external  body- wall 
changed  from  an  insensitive  hard  carapace  to  a  sensitive  mobile  covering. 
The  way  that  the  protective  mechanism  comes  into  play  is  by  exalting  the 
sensitiveness  of  reflexes.  Thus  if  an  organ  suffer  injury,  as  by  inflamma- 
tion, the  surrounding  portion  of  the  external  body-wall  immediately  has  its 
protective  functions  exalted.  This  is  usually  accomplished  by  increased 
sensitiveness  of  the  skin  and  underlying  structures,  so  that  touch  arouses 
at  once  a  strong  and  vigorous  contraction  of  the  protective  muscles.  These 
muscles  themselves  become  much  more  sensitive  to  pain,  and,  as  painful 
stimuli  are  the  most  provocative  causes  of  reflexes,  acutely  tender  muscles 
may  remain  permanently  contracted. 

To  illustrate  the  meaning  and  purpose  of  visceral  pain  and  allied  pheno- 
mena, a  case  of  gastric  ulcer  may  be  taken.  The  ulcer  may  be  situated  on 
the  posterior  wall  and  at  the  cardiac  orifice  of  the  stomach,  while  the  sensation 
of  pain  is  referred  to  the  epigastrium.  Here  the  skin  and  muscles  may  be 
found  exceedingly  tender  to  touch  and  light  pressure.  The  reflex  contraction 
of  the  underl3dng  recti  muscles  is  extremely  lively  and  powerful.  If  you  try 
gently  to  palpate  the  stomach,  these  muscles  at  once  become  so  strongly 
contracted  that  it  is  utterly  impossible  to  feel  what  is  underneath.  What 
is  nature  doing  ?  Manifestly  it  is  interposing  a  most  efficient  barrier  between 
the  intruding  hand  and  the  diseased  organ — the  whole  being  a  protective 
mechanism.  Had  the  stomach  only  been  sensitive,  the  hand  would  have 
reached  the  stomach,  but  by  the  reflex  mechanism,  the  external  body-wall 
is  made  sensitive,  and  the  powerful  reflex  contraction  of  the  muscles  effec- 
tively guards  the  stomach  from  injury.  The  same  protective  mechanism 
is  involved  in  joint-disease.  Thus  the  shoulder- joint  may  be  found  immobile. 
Put  the  patient  under  chloroform  and  all  the  muscles  relax,  and  a  grating 
may  be  detected  on  moving  the  joint.  It  is  evident  that  here  the  injured 
joint  required  protection,  and  the  muscles  responded  to  their  first  and 
primitive  duty. 

Pain  itself,  Hilton  pointed  out,  has  the  same  purpose, — protection.  It 
commands  at  once  cessation  of  any  action  that  induces  it,  and  this  protective 
function  is  seen  nowhere  more  clearly  than  in  heart  affections. 

§  41.  Why  pain  is  referred  to  regions  remote  from  the  organ. — 
In  a  great  many  instances  the  pain  is  referred  to  situations  remote  from  the 
organ  giving  rise  to  it.     Thus  the  pain  of  biliary  colic  may  be  felt  in  the 


REFLEX,  OR  PROTECTIVE  PHENOMENA 


39 


epigastrium,  the  pain  of  renal  colic  in  the  testicle,  the  pain  of  heart  affections 
in  the  arm. 

The  reason  for  this  is  that  in  the  course  of  development  the  tissues, 
that  in  a  low  scale  of  Hfe  immediately  covered  the  organ,  have  been  dis- 
placed. Thus,  the  pain  felt  in  the  testicle  in  renal  calculus  is  due  to  the  fact 
that  in  its  journey  down  to  the  scrotum  the  coverings  of  the  testicle  receive 
a  tw4g  from  the  first  lumbar  nerve,  from  which  the  kidney  is  also  innervated, 
and  when  the  centre  of  this  nerve  in  the  spinal  cord  is  stimulated,  as  in 
renal  calculus,  the  pain  is  felt  in  the  testicle,  and  exquisite  pain  may  be 
eUcited  on  pressing  the  testicle.  On  the  other  hand,  one  never  finds  the 
skin  of  the  scrotum  hyperalgesic  in  these  cases,  but  only  the  deep  covering 
of  the  testicle,  because  the  scrotum  is  supplied  by  the  sacral  nerves. 


LS9 


s  la 


Fig.  9.  Diagi-ammatic  representation  of  a  primitive  vertebrate  animal  to  show  the  distri- 
bution of  the  sensory  nerves.  For  clearness  of  comparison  the  number  of  segments  is  repre- 
sented to  be  the  same  as  in  man,  and  the  heart  occupies  the  same  position.  Each  nerve  is 
shoAvn  as  limited  in  its  distribution  to  one  segment  (after  Ross). 

§  42.  The  relationship  of  the  heart  to  sensory  nerves.— In  order 
to  appreciate  the  mechanism  of  the  pain  felt  in  affections  of  the  heart,  the 
manner  in  which  the  upper  dorsal  nerves  come  to  be  distributed  should  be 
borne  in  mind.  Ross  *^  has  pointed  out  that  in  the  primitive  vertebrates, 
before  the  development  of  the  limbs,  each  spinal  nerve  is  distributed  seg- 
mentally  round  one  half  of  the  body  (Fig.  9).  The  upper  dorsal  nerves 
are  therefore  entirely  distributed  over  the  body-wall  and  to  the  tissues 
covering  the  heart.  The  upper  limbs,  as  they  bud  out  from  the  trunk  in 
their  development,  drag  with  them  away  from  the  trunk  portions  of  the 
cervical  and  upper  dorsal  nerves,  so  that  parts  of  the  first  and  second  dorsal 
nerves  are  distributed  to  the  ulnar  border  of  the  forearm  and  inner  surface 
of  the  upper  arm.  Thus,  a  stimulus  originating  in  the  heart  and  affecting 
the  cord  area  of  the  first  and  second  dorsal  nerves,  would  be  felt  as  pain  in 
the  lowly  vertebrate  over  the  heart,  whereas  in  man  it  would  be  felt  in  the 
upper  arm  or  in  the  forearm  (Fig.  10). 

This  peculiar  distribution  of  the  nerves  to  the  chest  and  arm,  resulting 
from  the  development  of  the  limbs,  provides  a  unique  field  for  observing 


40 


DISEASES  OF  THE  HEART 


the  mechanism  of  many  nerve  processes.  The  character  of  the  field  can  be  seen 
in  the  distribution  of  the  shaded  area  in  Figs.  10,  and  12  (p.  51),  which  represent, 
the  one  the  distribution  of  the  eruption  in  a  case  of  herpes  zoster  affecting 
the  spinal  ganglia  of  the  eighth  cervical,  first  and  second  dorsal  nerves, 

and  the  other  the  area  in  which  pain  was  felt, 
and  in  which  the  skin  was  hyperalgesic  in  a  case 
with  the  symptoms  of  angina  pectoris.  The 
existence  of  these  and  similar  associated  areas 
has  been  demonstrated  by  a  variety  of  methods 
clinically,  experimentally,  and  by  dissection. 

We  know  that  the  efferent  cardiac  fibres  of 
the  sympathetic  pass  out  of  the  spinal  cord 
with  the  upper  dorsal  nerves.  Although  it 
is  impossible  experimentally  to  demonstrate 
the  region  of  the  spinal  cord  to  which  the 
afferent  nerves  pass,  clinical  observation  pro- 
vides ample  evidence,  and  this  evidence  demon- 
strates that  the  afferent  nerves  pass  into  the 
cord  at  the  same  regions  from  which  the 
efferent  pass  out. 

The  usual  description  given  of  the  pain  in 
angina  pectoris  is  that  it  is  felt  in  the  heart  and 
shoots  into  the  arm,  or  that  there  are  two  pains, 
a  local  pain  in  the  heart,  and  a  referred  pain  in 
the  arm.  If,  however,  a  careful  analysis  be 
made  of  aU  the  symptoms  present,  facts  will  be 
found  that  practically  demonstrate  that  in  angina 
pectoris  there  is  but  one  kind  of  pain,  and  that 
its  production  is  in  accordance  with  the  law 
I  have  attempted  to  establish,  namely,  that  it  is 
a  viscerosensory  reflex.  It  is  not  in  every  case 
that  one  is  able  to  demonstrate  the  truth  of  this 
hypothesis,  but  the  conclusions  drawn  from 
observations  made  in  suitable  cases  may  legitimately  b'e  applied  to  others. 
Shortly,  these  observations  are,  that  the  pain  in  the  very  gravest  cases 
may  be  felt  in  regions  distant  from  the  heart,  as  in  the  left  arm  ;  that 
this  pain  is  identical  in  character  with  that  felt  over  the  heart ;  that  the 
pain  may  originally  start  in  parts  distant  from  the  heart  and  gradually 
approach  and  persist  over  the  heart,  and  lastly,  that  the  tissues  of  the 
external  body-waU  over  the  heart  may  be  found  extremely  hyperalgesic 


Fig.  10.  The  dotted  area 
shows  the  distribution  of  an 
eruption  due  to  herpes  zoster 
in  the  peripheral  distribution 
of  the  eighth  cervical,  first  and 
second  dorsal  nerves.  There 
was  also  a  small  patch  of  erup- 
tion over  the  left  scapular  spine. 


REFLEX,  OR  PROTECTIVE  PHENOMENA  41 

after  the  pain  has  passed  away.  From  this  last  fact  it  is  inferred  that, 
inasmuch  as  the  seat  of  pain  corresponds  to  the  region  of  hjrperalgesia, 
therefore  the  pain  was  felt  by  the  hyperalgesic  nerves.  To  assume  otherwise 
is  to  ignore  a  principle  that  explains  satisfactorily  the  sensation  of  pain 
wherever  arising. 

§  43.  The  viscero-motor  reflex — So  far  I  have  dealt  mainly  with 
the  viscero-sensory  reflex,  but  no  less  striking  evidence  can  be  found  of  the 
viscero-motor  reflex  among  the  group  of  symptoms  included  in  the  term 
'  angina  pectoris  '.  Some  would  limit  the  term  '  angina  pectoris  '  to  that 
class  of  cases  where,  in  addition  to  the  pain,  there  is  a  sense  of  constriction 
in  the  chest,  amounting  to  the  sensation  at  times  as  if  the  chest  were  gripped 
in  a  vice,  or  as  if  the  breast  bone  would  break.  I  am  convinced  that  these 
sensations  arise  from  spasm  of  the  intercostal  muscles,  and  correspond  to 
the  hard  contraction  of  the  flat  abdominal  muscles  in  affections  of  the 
abdominal  viscera.  If  one  watch  a  case  of  what  is  called  '  muscular  rheu- 
matism ',  where  the  intercostal  muscles  are  affected,  and  where  these  muscles 
are  stimulated  by  the  slightest  movement  to  violent  cramp-Uke  contractions, 
one  cannot  but  be  struck  by  the  resemblance  to  the  description  given  by 
the  '  gripping  '  sensation  experienced  by  patients  suffering  from  certain 
affections  of  the  heart.  I  have  watched  the  attacks  in  such  cases,  and  could 
find  no  difference  between  them  and  those  where  the  sense  of  contraction 
was  the  chief  symptom  in  heart  disease. 

The  viscero-motor  reflex  may  be  present  alone,  or,  as  is  more  commonly 
the  case,  it  may  be  associated  with  the  pain.  The  purely  viscero-motor 
reflex  is  seen  best  in  the  elderly,  where  it  may  be  considered  a  symptom 
of  one  form  of  the  terminal  affections  of  the  heart  due  to  cardio-sclerosis 
or  old  age.  I  have  found  it  a  precursor  of  steadily  advancing  cardiac  weak- 
ness, and  although  for  a  time  considerable  rehef  may  be  afforded,  the  changes 
in  the  heart  are  so  advanced  that  in  the  nature  of  things  only  one  end  can 
be  looked  for.    In  such  cases  pain  may  be  absent. 

§  44.  Vagal  sensory  reflex — So  far  the  symptoms  I  have  dealt  with 
have  been  mainly  concerned  with  the  reflexes  connected  with  the  sympathetic 
nerve  supply.  Equally  instructive  though  less  frequent  symptoms  can  be 
shown  to  arise  from  stimulation  of  the  vagus.  At  its  centre  in  the  medulla 
this  nerve  is  in  near  relationship  to  the  upper  cervical  nerves,  and  it  would 
seem  more  particularly  to  the  sensory  nerves  supplying  the  sterno-mastoid 
and  trapezius  muscles.  Not  only  can  these  muscles  become  extremely 
hyperalgesic  in  various  heart  affections,  but  the  pain  from  heart  affection 
may  be  felt  in  the  region  of  distribution  of  the  cervical  nerves.  Pain  may 
also  be  felt  during  an  attack  of  angina  pectoris  in  the  gums  and  throat— 


42  DISEASES  OF  THE  HEART 

due  to  a  radiation  of  the  stimulus  from  the  vagus  to  the  centre  of  the 
fifth  nerve. 

Other  very  striking  reflexes  are  sometimes  met  with  in  an  attack  of 
angina  pectoris.  Thus  during  or  after  an  attack,  an  abundant  flow  of  saUva 
and  the  secretion  of  large  quantities  of  pale  urine  may  occur  ;  both  symptoms 
I  suggest  are  due  to  reflex  stimulation  of  the  floor  of  the  fourth  ventricle. 

There  are  also  good  grounds  for  attributing  some  forms  of  dyspnoea  to 
reflex  stimulation  from  the  heart. 

§  45.  Conditions  in  which  angina  pectoris  is  induced If  a  large 

number  of  cases  be  studied,  symptoms  of  angina  pectoris  will  be  found  to 
arise  in  patients  with  the  most  diverse  forms  of  lesion,  and  even  in  patients 
without  any  evidence  of  cardiac  disease.  From  among  a  number  of  con- 
ditions, I  select  the  following  :  Cases  of  (1)  aortic  aneurysm,  (2)  aortic 
valvular  disease,  (3)  atheroma  of  the  coronary  arteries,  (4)  myocardial 
degeneration  or  enfeeblement  of  the  heart  muscle  from  poor  nourishment 
or  over-exertion,  (5)  increased  arterial  pressure  of  the  elderly  (usually 
associated  with  3  and  4). 

It  would  seem  that  identical  symptoms  produced  from  conditions  so 
diverse  cannot  be  directly  due  to  the  organic  lesion,  to  the  aortic  aneurysm, 
to  the  disease  of  the  coronary  artery,  or  to  the  increased  peripheral  resis- 
tance.   We  must  therefore  look  for  a  cause  common  to  all  five  conditions. 

§  46.  Conditions  giving  rise  to  attacks  of  angina  pectoris In  order 

to  find  what  this  common  cause  may  be,  consideration  of  the  conditions  giving 
rise  to  an  attack  of  angina  pectoris  will  help  materially.  In  the  first  place, 
it  is  to  be  noted  that  angina  pectoris  in  the  five  conditions  cited  appears 
as  a  late  symptom,  after  the  heart  has  been  struggling  a  long  time  against 
obstacles  opposed  to  its  efficient  action,  or  after  the  nutrition  of  the  muscle 
has  been  impaired  by  gross  pathological  changes  in  the  coronary  artery^ 
or  when  the  muscle-fibres  have  become  impaired  through  slowly  advancing 
degeneration  of  the  fibres.  We  find,  further,  that  many  patients  when  at 
rest  do  not  suffer  from  pain,  but  that  any  cause  inducing  increased  work 
on  the  heart  provokes  an  attack.  Bodily  exertion  in  any  form,  excitement, 
increased  peripheral  resistance  (as  in  exposure  to  cold  air),  may  bring  on 
directly  an  attack  of  angina  pectoris.  That  is  to  say,  in  predisposed 
individuals  all  circumstances  that  throw  more  work  on  the  left  ventricle 
induce  an  attack  of  angina  pectoris. 

§  47.  Association  of  angina  pectoris  with  exhaustion  of  the  muscle 
of  the  heart — Such  considerations  lead  to  the  conclusion  that  angina  pec- 
toris arises  from  certain  conditions  of  the  muscular  substance  of  the  heart,, 
when  the  contraction  meets  with  a  resistance  greater  than  it  can  easily  and 


REFLEX,  OR  PROTECTIVE  PHENOMENA  43 

efficiently  overcome,  whether  a  fairly  strong  muscle  struggles  against  an 
increased  resistance  (as  when  there  is  great  peripheral  resistance  or  a  narrowed 
aortic  orifice),  or  when  a  weak  or  degenerated  muscle  has  opposed  to  its  con- 
traction a  normal  or  even  a  lowered  pressure,  but  a  pressure  greater  than  the 
Aveakened  muscle  can  readily  overcome. 

§  48.  Association  of  angina  pectoris  with  impairment  of  the  func- 
tion of  contractility — If  we  inquire  what  function  of  the  muscle-fibres  is 
concerned  in  the  production  of  angina  pectoris,  we  shall  find  additional 
confirmation  for  the  foregoing  conclusion. 

I  shall  later  deal  very  fully  with  the  fact  that  affections  of  certain  functions 
of  the  muscle-fibres  (Gaskell's  functions  ^2^)  can  be  demonstrated  by  means 
of  graphic  records  of  the  cardiac  movements.  I  have  taken  a  large  number 
of  tracings  from  patients  who  have  suffered  from  angina  pectoris — during 
the  attacks  and  when  free  from  pain — and  an  analysis  of  these  tracings 
enables  me  to  say  with  confidence  that  angina  pectoris  can  occur  when  the 
excitabihty,  the  conductivity,  and  the  power  to  produce  a  rhythmical 
stimulus  are  unimpaired.  There  only  remain  now  the  functions  of  tonicity 
and  contractility.  The  evidence  of  failure  of  the  function  of  tonicity  is 
mainly  shown  in  the  dilatation  of  the  heart,  and  typical  attacks  of  angina 
pectoris  frequently  occur  in  hearts  perfectly  normal  in  size.  Therefore  angina 
pectoris  may  occur  without  any  evidence  of  the  impairment  of  the  function 
of  tonicity.  Seeing,  then,  that  angina  pectoris  can  occur  in  patients  when 
four  out  of  five  functions  of  the  heart  muscle  are  demonstrably  intact,  we 
are  led  to  inquire  whether  angina  pectoris  may  not  be  due  to  an  impairment 
of  the  remaining  function,  that  is,  contractility.  When  we  come  to  look  for 
facts  that  have  a  bearing  on  this  question  we  find  :  (a)  an  a  'priori  evidence 
in  the  fact  that  this  is  the  function  directly  concerned  in  suppljdng  the 
motive  force  to  the  circulation  of  the  blood,  and  that  it  is  the  function  that 
will  necessarily  become  exhausted  when  an  excessive  resistance  is  opposed 
to  the  contraction  of  the  heart  muscle  ;  (&)  the  symptoms  associated  with 
and  the  conditions  giving  rise  to  the  characteristic  sign  of  depressed  con- 
tractility (pulsus  alternans),  are  of  a  similar  nature  to  the  symptoms  in 
angina  pectoris  ;  (c)  angina  pectoris  may  be  associated  Avith  the  pulsus 
alternans  ;  {d)  in  other  hollow  organs  severe  pains  are  evoked  by  contraction 
of  the  muscle- wall. 

From  this  line  of  reasoning  I  would  suggest  that  angina  pectoris  is  an 
evidence  of  exhaustion  of  the  function  of  contractility. 

§  49.  Summation  of  stimuli  as  a  cause  of  angina  pectoris. — 
The  fundamental  functions  of  the  heart  muscle  correspond  to  those  of  other 
involuntary  muscles  that  form  the  walls  of  hollow  organs  ;    these  functions 


44  DISEASES  OF  THE  HEART 

being  modified  to  suit  its  special  work.  Like  the  other  viscera,  the  heart 
is  insensitive  when  stimulated  in  a  manner  that  provokes  pain  when  applied 
to  the  tissues  of  the  external  body-wall.  I  may  point  out  that  a  prolonged 
strong  contraction  of  a  hollow  organ  can  produce  pain,  and  that  this  is 
undoubtedly  the  cause  of  the  severe  pain  associated  with  renal  calculus,  gall- 
stones, spasm  of  the  bowel,  and  uterine  contractions.  Can  the  heart  give 
rise  to  pain  in  a  similar  manner  ?  On  account  of  the  modification  of  its 
functions,  the  heart  cannot  pass  into  a  prolonged  state  of  contraction. 
Immediately  it  contracts,  the  function  of  contractihty  is  abolished  and  the 
muscle  passes  at  once  into  a  state  of  relaxation,  and  for  this  reason  the  pain 
cannot  be  produced  by  a  '  spasm  of  the  heart  '.  But  I  suggest  that  the 
heart  muscle  may  produce  pain  when  it  is  confronted  with  work  greater 
than  what  it  can  readily  overcome — a  condition  which  produces  strong 
peristalsis  and  pain  in  other  hollow  viscera.  But  the  pain  in  the  heart 
arises  by  a  sUghtly  different  mechanism.  A  skeletal  muscle  will  contract 
in  obedience  to  stimulation  of  a  sensory  nerve  going  to  the  spinal  centre 
of  its  nerve,  if  a  stimulus  of  sufficient  strength  be  applied.  If  the  stimulus 
is  too  weak  no  contraction  follows,  but  if  this  weak  stimulus  be  frequently 
and  rapidly  repeated,  then  the  muscle  contracts  in  accordance  with  the 
law  of  the  summation  of  stimuli.  I  suggest  that  the  heart  muscle  induces 
pain  on  the  principle  of  summation  of  stimuli.  If  we  minutely  study  our 
cases  we  shall  find  that  the  pain  rarely  arises  at  the  first  exposure  of  the  heart 
to  the  effort  that  induces  the  pain  ;  sometimes  effort  has  been  undertaken 
a  few  minutes  before  the  pain  comes  on,  and  in  certain  cases  it  may  not 
come  on  for  hours  after  the  causal  exertion  has  ceased.  From  such  observa- 
tion we  can  infer  that  the  heart  muscle  was  exhausted  by  the  exertion, 
and  so  great  was  the  exhaustion  of  the  reserve  force  that  the  heart  was 
unable  to  regain  its  reserve  with  cessation  of  effort,  so  that  the  exhaustion 
persisted  till  it  culminated  in  an  attack  of  angina  pectoris. 

The  reasonableness  of  this  explanation  will  be  more  apparent  after  dealing 
specially  with  the  symptoms  of  angina  pectoris  in  individual  cases. 


CHAPTER  VII 

Angina  Pectoris 

§  50.  Conditions  predisposing  to  an  attack. 

51.  Conditions  inducing  an  attack. 

52.  Character  and  duration  of  an  attack. 

53.  The  sjrmptoms  present  during  an  attack  :   pain,  constriction 

of  the  chest,  sense  of  impending  death. 

54.  The  state  of  the  heart  and  arteries. 

55.  The  s3Tnptoms  present  after  an  attack. 

56.  Establishment  of  a  tendency  to  recurrent  attacks. 

57.  Prognosis. 

58.  Treatment. 

In  Chapter  VI,  I  give  the  reasons  for  assuming  that  the  symptom  complex 
called  Angina  Pectoris  belongs  to  the  class  of  reflex  protective  phenomena 
where  the  symptoms  are  evoked  by  a  viscus  reflexly  stimulating  certain 
areas  in  the  central  nervous  system.  The  stimulus  from  the  heart  to  the 
spinal  cord  irritates  the  nerve-cells  in  close  proximity  to  the  nerve  conveying 
the  stimulus  from  the  heart.  The  nerves  thus  irritated  respond  and  exhibit 
the  evidence  of  their  peculiar  function — sensory  nerves,  by  pain  felt  in  their 
peripheral  distribution,  motor  nerves,  by  contraction  of  the  muscles.  In 
this  way  we  get  the  peculiar  distribution  of  pain  in  angina  pectoris,  and  the 
sense  of  constriction  of  the  chest-wall.  This  violent  stimulation  of  the 
spinal  cord  may  leave,  after  its  subsidence,  an  irritable  focus  in  the  cord, 
rendering  that  portion  of  the  cord  more  susceptible  to  stimulation,  so  that 
it  becomes  easier  for  future  attacks  of  angina  pectoris  to  be  provoked.  This 
irritable  focus  can  be  demonstrated  to  exist  in  some  patients  by  the  hyper- 
algesic  state  of  the  skin  and  muscles,  and  other  subcutaneous  tissues  in  the 
region  where  the  pain  was  felt.  So  sensitive  may  this  irritable  focus  become, 
that  an  attack  of  angina  pectoris  may  be  provoked  by  a  stimulation  reaching 
the  focus  from  regions  other  than  the  heart.  I  have  further  suggested  in  the 
foregoing  chapter  that  these  phenomena  are  not  the  outcome  of  the  gross 
lesion  found  in  cases  of  angina  pectoris,  but  are  due  to  the  exhaustion  of 
the  contractile  function  of  the  heart  muscle.  If  this  view  be  kept  in  mind, 
the  examination  of  patients  is  greatly  facilitated,  and  the  grounds  for 
a  rational  diagnosis,  prognosis,  and  treatment  are  laid. 

§  50.  Conditions  predisposing  to  an  attack. — That  a  muscle  should 


46  DISEASES  OF  THE  HEART 

evoke   disagreeable  symptoms  when  over-fatigued  is   a  principle   applic- 
able   to  all   muscular  structures   of   the   body.     The  peculiar  functional 
attributes  of   the  heart    muscle   imply  a  modified  method  of   exhibiting 
these  disagreeable  symptoms,  which  I  have  dealt  with  in  Chapter  VI, 
showing  how  in  many  cases  it  is  probably  due  to  the  law  of  summation  of 
stimuli.     In  looking  at  the  coronary  arteries  in  certain  typical  cases  of 
angina  pectoris,  one  can  reasonably  infer  one  way  in  which  the  attacks 
are  brought  about.    In  some  cases  the  coronary  arteries  are  so  narrowed  as 
scarce  to  permit  the  entrance  of  a  pin.     During  life  the  stream  of  blood 
must  have  been  greatly  reduced,  and  if  it  were  sufficient  to  supply  the 
muscle  during  rest,  it  was  demonstrably  insufficient  while  the  heart  was 
in  a  state  of  activity.     In  this  respect  there  seems  to  be  a  distinct  affinity 
between  the  origin  of  the  pain  in  these  cases,  and  in  those  cases  of  what  is 
called  '  intermittent  claudication  ' — first  described  in  the  horse,  but  not 
infrequent  in  man.     In  one  of  my  cases  of  this  complaint,  for  two  years 
the  patient  could  not  walk  one  hundred  yards  before  he  had  to  stand  still 
and  rest  on  account  of  the  great  pain  in  the  legs  and  feet,  and  of  intense 
coldness  of  his  feet.     On  standing  a  few  minutes  the  pain  disappeared,  and 
his  feet  became  warmer.    Here  there  was  a  marked  atheromatous  degenera- 
tion of  the  arteries  of  the  leg,  and  the  supply  of  blood  was  sufficient  for  the 
muscles  when  at  rest,  but  contraction  of  the  muscles  demanded  a  greater 
supply  than  the  arteries  could  furnish,  with  the  result  that  the  exhausted 
muscles  became  painful,  and  the  diminished  supply  of  blood  to  the  skin 
caused  a  sense  of  coldness.    Ultimately  the  arterial  supply  became  so  slight 
that  gangrene  of  the  toes  set  in.     From  the  foregoing  illustrations  a  fairly 
safe  conclusion  can  be  drawn  as  to  the  manner  in  which  anginal  symptoms 
are  provoked.    It  can  further  be  safely  inferred  that  the  muscle  exhaustion 
may  arise  in  other  ways,  for  example,  when  the  nutrition  is  poor,  as  happens 
in  anaemic  and  badly  nourished  people.    The  heart  may  become  exhausted 
because  it  is  never  allowed  sufficient  time  to  recover  its  reserve  force,  as  in 
individuals  who  are  worried  and  overworked.     Or  exhaustion  may  arise 
from  obstruction  to  the  work  of  the  left  ventricle,  as  in  disease  of  the  aortic 
valves,  and  in  atheroma  of  the  arteries,  especially  when  accompanied  with 
partial    obliteration    of    the    capillary   field    (§    221).      In  these  cases  the 
disease  that  has  damaged  the  aortic  valves  and  arteries  has  at  the  same 
time  invaded  and  enfeebled  the  heart. 

In  addition  to  exhaustion  of  the  heart  muscle  as  a  cause  of  angina  pectoris, 
there  has  to  be  noted  this  further  fact,  that  angina  pectoris  arises  only  in 
connexion  with  exhaustion  of  the  left  ventricle.  The  symptoms  of  angina 
pectoris  are  invariably  associated  with  lesions  on  the  ventricular  side  of  the 


ANGINA  PECTORIS  47 

mitral  orifice.  In  a  few  cases  I  have  found  angina  pectoris  in  patients  with 
mitral  stenosis  after  violent  exertion,  but  it  is  to  be  noted  that  the  blood- 
supply  to  the  ventricle  is  limited  in  such  cases.  I  do  not  remember  having 
seen  a  case  of  angina  pectoris  with  free  mitral  regurgitation  unaccompanied 
by  affections  of  the  aortic  valves  ;  hyperalgesia  of  the  chest-wall  is,  however, 
fairly  common  when  there  is  also  dilatation  of  the  heart.  In  several 
instances  I  have  noted,  with  Broadbent  and  Musser,  the  complete  cessa- 
tion of  anginal  attacks  with  the  onset  of  free  mitral  regurgitation.  In 
such  cases  the  attacks  were  due  to  the  left  ventricle  struggling  to  overcome 
the  high  arterial  pressure,  and  the  cessation  was  due  to  the  dilatation 
of  the  heart  rendering  incompetent  the  mitral  valves,  and  thus  permitting 
the  ventricle  to  ease  its  load  (Chapter  XXVII).  Though  freedom  from 
attacks  of  angina  pectoris  was  thus  acquired,  a  great  fall  of  arterial  pres- 
sure resulted,  leading  to  dropsy  and  gradual  exhaustion  (Chapter  XXII). 

§  51.  Conditions  inducing  an  attack — Angina  pectoris  is  never  the 
outcome  of  an  acute  affection  ;  it  is  invariably  led  up  to  by  a  long  period  of 
gradual  exhaustion.*  The  onset  is,  in  the  majority  of  cases,  induced  by 
some  extra  effort  on  the  part  of  the  heart.  This  need  not  be  an  effort  of 
unusual  severity  ;  it  occurs  more  frequently  when  the  individual  is  using 
his  powers  in  a  way  which  formerly  required  no  very  marked  strain.  The 
cause  may  be  of  the  nature  of  bodily  exertion,  mental  excitement,  exposure 
to  cold  air,  or  anything  that  calls  for  more  work  on  the  part  of  the  heart. 
In  most  cases  the  attack  does  not  come  on  at  once,  unless  the  effort  is  per- 
sisted in,  as  in  walking  up  a  hill,  and  the  first  warnings  of  heart  exhaustion 
are  ignored.  The  attack  of  pain  may  not  come  for  some  minutes  or  even 
hours  after  the  causal  exertion  has  ceased,  and  when  the  patient  has  been 
resting  in  bed.  In  some  severe  cases  the  attack  of  pain  may  come  on  at 
intervals  when  the  patient  has  been  exposed  to  no  exertion,  particularly 
in  cases  where  the  attacks  have  been  frequent,  and  a  tendency  to  them  has 
been  established. 

§  52.  Character  and  duration  of  an  attack The  attacks  may  be 

so  shght  at  first  as  to  pass  almost  unnoticed,  and  it  is  only  after  they  become 
more  frequent  and  severe  that  the  patient's  attention  is  called  to  the  fact 
that  he  had  previously  experienced  some  discomfort.  In  the  more  simple 
cases  the  pain  may  not  be  very  severe,  and,  appearing  after  some  violent 
exertion,  may  never  again  show  itself.  Instead  of  pain  it  may  be  but  a  slight 
sensation  of  constriction  across  the  chest,  that  calls  for  a  deep  inspiration 

*  Except  in  cases  of  coronary  embolism,  of  which  there  are  several  cases  on  record  in 
which  attacks  of  angina  pectoris  were  evidently  due  to  the  plugging  of  a  coronary  artery 
(Garrod '  and  Parkes  Weber  "). 


48  DISEASES  OF  THE  HEART 

to  relieve  the  tension.  The  more  severe  attacks  imperatively  command 
a  cessation  of  all  efforts,  and  here  all  degrees  of  suffering  may  be  experienced. 
Dm-ing  the  attack  the  patient  may  stand  still  in  a  position  of  rigid  immo- 
biUty,  afraid  to  move  or  to  speak,  scarcely  daring  to  breathe,  or  he  may  kneel 
down  and  rest  his  head  on  a  chair,  or  roll  on  the  floor  in  an  extremity  of 
agony,  or  the  patient  may  become  unconscious  and,  in  rare  cases,  may  die. 
If  the  pain  is  located  in  the  arm,  he  may  nurse  it  across  his  chest,  rocking 
backwards  and  forwards.  The  face  may  become  pale  or  flushed,  and  beads 
of  perspiration  may  roU  down  the  forehead.  The  attack  may  terminate 
with  the  expulsion  of  air  from  the  stomach,  unconsciously  sucked  into  the 
stomach  during  the  attack  (§-64). 

In  most  cases  the  attack  lasts  for  a  few  seconds,  but  it  may  continue 
with  great  severity  for  several  hours,  yielding  only  to  large  doses  of  opium. 
Such  severe  cases  may  die  during  the  suffering. 

§  53.  The  symptoms  present  during  an  attack  of  angina  pectoris. — 
The  chief  symptom  is  pain  :  there  may  be  also  a  sense  of  constriction  across 
the  chest,  a  sense  of  suffocation,  and  a  sense  of  impending  death.  Occa- 
sionally other  reflexes  may  be  present,  such  as  a  flow  of  saUva  from  the 
mouth,  and  an  increased  secretion  of  urine.  These  symptoms  are  not  aU 
present  in  every  attack,  nor  are  they  always  present  in  the  same  degree. 
There  may  be  a  shght  pain  or  a  slight  sense  of  constriction  across  the  chest. 
Or  the  pain  may  be  of  the  utmost  severity,  with  constriction  of  the  chest 
so  violent  that  the  patient  feels  as  if  his  breast  bone  was  about  to  break. 

Pain. — Pain  is  usually  referred  to  some  portion  of  the  distribution  of 
the  upper  four  left  dorsal  nerves  in  the  chest  and  arm.  Sometimes  the  pain 
may  be  felt  as  low  as  the  distribution  of  the  sixth  dorsal  nerves  in  the  epigas- 
trium, and  as  high  as  the  eighth  and  seventh  cervical  in  the  ulnar  border 
of  the  forearm  and  hand.  It  is  rarely  felt  in  similar  areas  on  the  right  side, 
and  sometimes  it  is  felt  in  the  neck  and  back  of  the  head,  in  the  upper  cervical 
nerves,  whose  roots  are  in  close  association  with  the  vagus.  The  pain  is 
usually  felt  across  the  chest,  and  may  remain  stationary  there,  or  it  may 
radiate  in  a  very  definite  manner  into  the  axilla,  and  down  the  arm  to  the 
ulnar  border  of  the  forearm  and  hand.  When  it  does  this  it  may  stop  for 
a  brief  period  in  the  upper  arm  or  forearm,  and  be  felt  there  most  violently. 
On  the  other  hand,  the  pain  may  start  in  the  arm  and  radiate  to  the  chest, 
where  it  remains  with  great  severity  for  a  time. 

Constriction  of  the  Chest. — Arising  along  with  the  pain,  or  following  it,  or 
quite  independent  of  the  sensation  of  pain,  is  a  sense  of  constriction,  which 
I  have  reasoned  is  due  to  the  reflex  stimulation  of  the  intercostal  muscles. 
It  may  be  so  slight  as  to  be  felt  only  as  a  mere  tightness  across  the  chest 


ANGINA  PECTORIS  49 

following  exertion,  or  it  may  grip  the  chest  so  firmly  that  the  patient  has 
to  stand  still  and  take  a  great  deep  inspiration  to  relieve  the  spasm  of  the 
muscles.  In  its  most  violent  form  it  adds  greatly  to  the  suffering  of  the 
jjatient  when  pain  is  also  present.  Thus  a  man  aged  forty-eight,  who  had 
violently  exerted  himself,  felt  a  pain  in  his  chest  come  on  gradually  some 
minutes  after  the  exertion.  As  the  pain  increased  he  called  on  me,  and 
I  asked  him  if  he  felt  his  chest  constricted.  He  said  '  No  '.  A  few  hours 
later,  the  pain  increased  in  severity  ;  then  suddenly  he  felt  his  chest 
gripped  with  a  violence  so  great  that  it  added,  he  said,  indescribably  to 
the  terror  of  his  suffering.  It  was  only  relieved  by  large  doses  of  opium. 
Next  day  he  felt  for  a  short  time  when  in  bed  as  though  that  '  awful  gripping 
were  coming  on  ',  and  he  lay  for  ten  minutes  with  perspiration  pouring  off 
him,  in  the  dread  of  its  return. 

Feeling  of  impending  dissolution. — This,  I  presume,  is  the  result  of 
violent  stimulation  of  the  nervous  system  comparable  to  what  happens 
when  any  other  viscus  is  violently  stimulated,  as  after  a  blow  in  the  epigas- 
trium, or  on  the  testicle.  On  rare  occasions  the  patient  faints  during  an 
attack,  and  in  one  instance  a  patient  of  mine  never  recovered,  but  died 
during  the  faint. 

§  54.  The  state  of  the  heart  and  arteries — The  observations  of 
NothnageP^  that  contraction  of  the  arterioles  may  precede  an  attack  of  angina 
pectoris,  and  of  Lauder  Brunton^  that  the  peripheral  arteries  may  contract 
during  an  attack  of  angina  pectoris,  have  led  to  some  misapprehension 
regarding  the  circulation  in  this  condition.  I  have  had  the  opportunity 
of  examining  a  large  number  of  patients  during  attacks  of  angina  pectoris, 
in  some  of  whom  the  onset  occurred  immediately  after  exertion,  in  others 
some  hours  after  exertion  ;  in  others  the  attacks  have  conle  on  suddenly  when 
the  patient  was  in  bed.  I  have  taken  a  large  number  of  sphygmographic 
tracings  and  a  few  blood-pressure  observations  during  these  attacks,  and  have 
never  found  a  single  case  where  the  arteries  were  constricted  in  the  manner 
sometimes  described  (see  illustrative  cases  in  Appendix  I).  In  six  cases 
where  the  patient  was  seized  with  the  pain  in  bed,  and  died  during  the  attack, 
there  was  not  the  sHghtest  sign  of  contracted  arteries.  In  one  of  these  cases 
I  measured  the  blood-pressure  during  an  attack  shortly  before  his  death, 
and  found  that  the  pressure  had  fallen  considerably.  I  have  seen  and 
carefully  studied  a  few  cases  of  Nothnagel's  '  vaso-motor  angina  pectoris  ', 
and  can  positively  state  that  they  come  under  a  different  category  from 
the  more  common  forms  of  angina  pectoris  due  to  disease  of  the  coronary 
arteries  (§  66).  I  can  only  infer  that  cases  of  arterial  spasm  are  very  excep- 
tional, and  their  description,  fostered  by  the  relief  obtained  by  the  adminis- 

MACKENZIE  -c^ 


50  DISEASES  OF  THE  HEART 

tration  of  amylnitrite,  has  given  quite  a  wrong  conception  in  regard  to  the 
conditions  inducing  an  attack  of  angina  pectoris.  I  have  found  during 
these  attacks  the  pulse  became  small,  soft,  and  scarcely  perceptible,  from 
weakness  of  the  heart,  the  heart  sounds  becoming  very  faint.  I  have  also 
found .  acceleration  of  the  heart's  rate — in  one  case  very  considerable, — 
and  occasionally  the  occurrence  of  an  extra-systole,  followed  sometimes  by 
a  characteristic  pulsus  alternans.  In  a  few  cases  irregularities  have  occurred 
whose  nature  I  have  not  been  able  to  determine  satisfactorily,  but  in  the 
vast  majority  of  cases  I  could  detect  no  change  in  the  heart  or  arteries, 
and  there  never  was  the  slightest  enlargement  of  the  heart  coming  on  during 
the  attack. 

§  55.  Symptoms  after  an  attack — The  patient  feels  greatly  exhausted 
after  the  attack  has  passed  off.  Sometimes  the  pain  does  not  completely 
disappear,  and  an  uneasy  painful  sensation  may  last.  The  end  of  an  attack 
may  coincide  with  the  expulsion  of  air  from  the  stomach,  and  as  this  is 
usually  accompanied  by  a  sense  of  relief,  the  attacks  are  often  supposed  to 
be  of  gastric  origin.  I  have  watched  these  patients,  and  have  no  doubt  that 
the  air  has  been  sucked  into  the  stomach  during  the  attack.  This  air  suction 
is  seen  most  characteristically  in  nervous  people,  especially  women,  and  is 
referred  to  more  fully  in  §  64.  Some  patients  have  a  desire  to  micturate, 
and  the  urine  secreted  is  always  abundant,  pale,  and  of  low  specific  gravity. 
In  some  patients  areas  of  hyperalgesia  of  the  skin  appear  in  some  portion 
of  the  field  in  which  the  pain  is  felt.  In  the  first  attacks  it  may  be  limited 
to  a  small  patch,  as  in  Fig.  11,  but  with  recurring  attacks  the  area  may  spread 
wherever  the  pain  is  felt,  as  in  Fig.  12. 

§  56.  Establishment  of  a  tendency  to  recurrence  of  the  attacks. — 
I  have  already  described  how  an  irritable  focus  may  be  produced  in  the  cord 
after  a  violent  stimulation  from  a  visceral  lesion  (shaded  area  in  Fig.  8,  p.  36). 
This  may  be  manifested  by  an  area  of  hyperalgesia  in  some  part  of  the 
body,  and  in  those  that  exhibit  this  hj^peralgesia  attacks  of  angina  pectoris 
come  on  with  very  little  provocation.  Even  when  there  is  no  distinct 
evidence  of  hyperalgesia,  the  stimulation  of  the  skin  or  the  movements  of 
the  muscles  of  the  arm  may  induce  an  attack.  I  have  on  several  occasions 
inadvertently  brought  on  an  attack  while  testing  the  sensibility  of  the  skin 
and  deeper  tissues  over  the  praecordium.  Visiting  a  patient  one  day,  who 
suffered  from  violent  attacks,  I  found  him  feeding  himself  entirely  with 
his  right  hand.  When  I  asked  him  why  he  did  not  use  his  left,  he  said  he 
was  afraid  to  do  so,  as  sometimes  the  movement  of  the  left  arm  induced 
an  attack.     He  died  a  few  hours  after,  during  an  attack. 

§  57.   Prognosis The  tragic  circumstances~surrounding  certain  cases 


ANGINA  PECTORIS 


51 


of  angina  pectoris  have  so  oppressed  the  profession  and  the  laity  that  an 
altogether  exaggerated  opinion  has  been  formed  of  the  gravity  of  this  com- 
plaint. If  it  be  realized  that  angina  pectoris  is  but  the  expression  of  an 
exhausted  muscle,  and  that  the  exhaustion  may  arise  from  any  cause  that 


Fig.  11.  The  shaded  area  shows 
the  position  of  a  patch  of  cutaneous 
hyperalgesia  after  the  first  attack  of 
angina  pectoris. 


Fig.  12.  The  shaded  area  shows  the  dis- 
tribution of  the  pain  and  cutaneous  h3rper- 
algesia  after  repeated  attacks  of  angina 
pectoris.  From  the  same  patient  as  Fig.  11 
(compare  the  shaded  area  with  the  distribution 
of  the  eruption  in  Fig.  10).  The  roman 
numbers  refer  to  the  nerves  implicated,  viz.  i, 
II,  and  III — the  first,  second,  and  third  dorsal 
nerves,  and  viii,  the  eighth  cervical  nerve. 


overtaxes  the  heart,  a  truer  appreciation  of  the  meaning  of  the  symptoms 
will  be  obtained.  The  estimation  of  the  gravity  of  the  cases  does  not  depend 
upon  the  violence  of  the  symptoms.  A  severe  attack  is  not  necessarily 
serious,  nor  is  the  mildest  free  from  danger.  The  importance  of  the  symp- 
toms must  be  estimated  by  an  examination  of  the  conditions  that  have 
induced  the  muscular  exhaustion.      This  is,  as  a  rule,  not  a  matter  of 

E  2 


52  DISEASES  OF  THE  HEART 

much  difficulty,  if  one  carefully  searches  for  a  predisposing  cause.  The 
age  of  the  patient,  the  conditions  of  his  or  her  Ufe,  work,  worry,  nourish- 
ment, over-indulgence  in  tobacco,  and,  in  the  case  of  women,  the  number 
of  children  she  has  borne,  her  menstrual  functions,  all  lead  to  the 
recognition  of  the  nature  of  the  muscular  exhaustion.  If  the  probabilities 
point  to  the  absence  of  progressive  arterial  degeneration  and  degeneration 
of  the  heart  muscle,  the  patient  may  on  the  whole  be  assumed  to  have 
a  favourable  future.  If  one  has  reason  to  suspect  that  the  symptoms  have 
appeared  in  the  early  days  of  cardio-sclerosis,  when  the  patient,  ignoring 
the  limitation  of  his  powers,  follows  the  manner  of  his  life  pursued  in 
vigorous  manhood,  then  the  probabilities  are  that,  with  rest  and  care,  the 
heart  wiU  recover  from  its  exhaustion,  and  be  able  to  carry  on  its  work 
for  many  years  in  comfort.  Where  the  prognosis  is  most  serious  is  when  it 
occurs  with  marked  evidence  of  general  arterial  degeneration,  and  where 
there  is  little  response  to  treatment,  and  where  the  attacks  are  induced 
with  slight  provocation.  These  are  the  circumstances  that  would  lead 
one  to  look  gravely  upon  this  condition.  But  even  when  cases  are  so  severe 
that  for  months  a  patient  may  scarcely  be  able  to  walk  across  the  floor 
without  inducing  an  attack,  rest  for  a  long  period  may  restore  the  heart  and 
induce  a  cessation  of  the  symptoms  ;  otherwise  the  condition  arrived  at  is 
practically  beyond  the  possibility  of  recovery. 

§  58.  Treatment. — Treatment  naturally  divides  itself  into  two  heads, 
namely,  the  improvement  of  the  condition  of  the  heart,  and  the  giving  of 
relief  during  an  attack. 

Improvement  of  the  condition  of  the  heart. — For  the  first  of  these  it 
must  be  borne  in  mind  that  the  attack  is  the  expression  of  an  exhausted 
muscle,  and  the  treatment  requires  a  careful  inquiry  into  the  conditions 
inducing  that  exhaustion.  First  and  foremost,  a  stop  must  be  put  to 
that  form  of  exertion  which  has  induced  the  attack,  and  any  other 
conditions  that  predispose  to  it  must  be  avoided,  such  as  work,  worry, 
sleeplessness,  over-indulgence  in  food  and  alcohol,  tobacco,  and  so  forth. 
The  next  step  is  to  place  the  heart  in  such  a  position  that  it  will  regain 
its  reserve  force,  that  is,  the  heart  must  be  given  less  to  do.  This  does 
not  necessarily  mean  that  the  patient  should  rest  in  bed,  but  he  should 
restrict  his  movements  as  much  as  possible.  Here  the  habits  and  condition 
of  the  patient  will  have  to  be  considered,  and  each  individual  separately 
treated.  To  stop  an  individual  altogether  from  his  work  and  engagements 
may  be  most  serious.  It  is  best,  as  a  rule,  to  permit  him  to  follow  some 
particular  kind  of  work  that  does  not  put  a  strain  upon  his  heart.  When 
feasible,  a  complete  change  of  habits  and  life,  as  free  from  over-exertion  as 


ANGINA  PECTORIS  53 

possible,  is  most  beneficial,  such  as  a  good  holiday  spent  in  the  manner  that 
affords  the  maximum  of  enjoyment  and  requires  the  minimum  of  effort. 
In  the  cases  that  do  not  yield  to  such  limited  restriction,  and  when  the  attacks 
are  demonstrably^  the  outcome  of  an  advanced  exhaustion  of  the  heart, 
then  absolute  rest  in  bed  is  necessary.  In  other  conditions  the  treatment 
should  follow  the  lines  that  I  have  laid  down  in  the  chapters  upon  treat- 
ment. Of  remedies  and  methods  supposed  to  cure,  the  name  is  legion. 
Happily  in  their  prescription  the  above  suggestions  are  also  included,  and  the 
benefit  so  accruing  is  too  often  attributed  to  the  remedy  or  method.  I  have 
in  several  individual  patients  tried  various  so-called  remedies,  and  I  find 
on  the  whole,  that  if  the  patient  is  not  worried,  has  plenty  of  sleep,  and 
leads  a  fairly  restful  life,  he  does  as  well  without  any  special  drug  treatment 
as  he  did  with  it. 

As  many  patients  of  a  neurotic  type  suffer  from  angina  pectoris  the  mental 
factor  should  always  be  considered.  The  term  angina  pectoris  conveys  to 
their  minds  such  fearful  associations,  that  they  readily  become  depressed 
and  miserable.  A  careful  study  of  each  case  will  show  that  in  the  majority 
the  attack  is  the  outcome  of  a  temporarily  exhausted  muscle  and  the  patient 
can  have  his  mind  relieved  by  the  assurance  that  the  prognosis  is  a  good 
one.  In  the  after-treatment  of  such  cases  careful  management  is  needed, 
in  order  that  they  should  not  always  be  reminded  of  their  complaint.  Hence 
systems  of  dieting,  where  the  patient  at  each  meal  has  to  reflect  if  the 
ingredients  are  injurious  to  his  heart,  should  be  rigidly  avoided.  Most 
dietetic  systems  are  the  outcome  of  a  fad,  and  based  on  an  imperfect  know- 
ledge of  digestive  and  metabolic  processes,  as  in  the  exclusion  of  common  salt 
and  lime  salts  from  the  meals.  For  the  same  reason  '  health  resorts  '  where 
people  congregate  and  discuss  their  ailments  should  be  avoided. 

Treatment  durmg  an  attack. — The  slighter  attacks  require  no  treat- 
ment. When  they  become  more  severe,  rapidly  acting  vasodilators  should 
be  administered,  such  as  hot  drinks,  hot  water  with  whisky  or  brandy,  and, 
best  of  all  and  most  speedy,  amylnitrite  by  inhalation.  This  drug  is  not 
successful  in  all  cases,  but  in  many  its  action  is  rapid,  and  the  relief  is 
generally  complete.  When  it  is  successful,  it  has  been  inferred  that  the 
patient  had  previously  constricted  arterioles,  or  increased  arterial  pressure, 
and  that  the  pressure  was  reduced,  and  so  the  heart  was  eased.  This  is 
not  the  full  explanation.  A  patient  with  cardio-sclerosis  had  an  attack  of 
angina  pectoris  in  my  consulting-room.  I  took  his  blood-pressure,  and 
found  it  190  mm.  Hg.,  and  then  administered  to  him  nitrite  of  amyl  :  it 
acted  instantaneously,  and  gave  him  perfect  relief.  After  fifteen  minutes 
I  again  took  his  blood-pressure,  and  found  that  it  had  risen  to  200  mm.  Hg. 


54  DISEASES  OF  THE  HEART 

Though  the  pressure  was  higher,  he  had  no  pain.  I  inferred  that  the  action 
was  similar  to  that  of  a  man  who  puts  on  a  hat  that  is  too  tight  ;  at  first 
there  is  no  pain,  but  gradually,  by  the  summation  of  stimuli,  discomfort 
comes  on  and  increases  in  intensity  ;  he  removes  the  hat  from  his  head, 
and  obtains  relief.  He  replaces  the  hat  in  the  same  position,  and,  although 
it  is  as  tight  as  before,  the  pain  has  permanently  disappeared  :  so  that  the 
temporary  removal  of  the  summating  stimuli  seems  to  be  the  reason  for 
the  relief  afforded  in  the  particular  case  mentioned. 

When  nitrite  of  amyl  fails  to  relieve  the  patient,  we  are  forced  to  use 
chloral  or  morphia  in  doses  sufficient  to  give  relief.  I  have  found  occasionally 
that  chloral  acts  beneficially  not  only  in  relieving  the  somewhat  long  attacks, 
but  in  preventing  the  attacks  recurring,  when  given  in  repeated  small  doses 
of  3-5  grains  and  also  when  given  at  night  to  induce  sound  sleep. 

In  advanced  cases  where  the  suffering  comes  on  mainly  at  night,  it  is 
occasionally  very  difficult  to  give  the  patient  relief.  Massive  doses  of  oxygen 
have  in  some  cases,  as  in  cardiac  asthma,  been  followed  by  marked  benefit, 
and  should  be  tried  (see  p.  279). 


CHAPTER   VIII 

Heart  Affections  and  a  Hypersensitive  Nervous  System 

§  59.  Reaction  of  visceral  disease  on  the  central  nervous  system. 

60.  Pseudo-angina  pectoris,  a  useless  and  misleading  term. 

61.  Exaggerated  sensory  phenomena  with  and  without  valvular  disease. 

62.  Exaggerated  sensory  phenomena  in  early  cardio-sclerosis. 

63.  Characteristics  of  the  sensory  phenomena. 

64.  Air  suction. 

65.  The  circulatory  symptoms  in  the  X  disease. 

66.  Vaso-motor  angina  pectoris. 

67.  Prognosis. 

68.  Treatment. 

It  not  infrequently  happens  that  the  most  common  forms  of  disease 
are  the  most  difficult  to  describe.  I  attempt  here  the  analysis  and  explana- 
tion of  the  symptoms  present  in  certain  cases  which  are  frequently  met  in 
actual  practice.  As  the  symptoms  present  great  variety  in  number  and 
intensity,  numerous  attempts  have  been  made  to  divide  them  into  groups, 
and  we  find  them  under  various  guises,  as  neurotic  hearts,  cardiac  neuroses, 
cardiac  neurasthenia,  pseudo-angina  pectoris.  I  have  endeavoured  to 
find  the  underlying  principles  which  provoke  these  manifold  symptoms, 
as  their  due  appreciation  is  of  prime  importance  in  the  management  of 
these  cases. 

§  59.  Reaction  of  visceral  disease  on  the  central  nervous  system. — 
In  describing  the  symptoms  of  angina  pectoris  (Chapters  VI  and  VII),  I 
have  endeavoured  to  show  that  the  symptoms  arise  from  a  reflex  stimulation 
of  the  central  nervous  system.  But  the  heart  and  the  nervous  system  can 
react  upon  one  another  in  other  ways  than  by  reflex  stimulation.  In  heart 
affections,  as  in  affections  of  all  other  viscera,  there  is  a  tendency  for  the 
central  nervous  system  to  become  hypersensitive  (I  use  this  word  for  want 
of  a  better)  whereby  symptoms  of  nervous  origin  are  readily  evoked.  This 
applies  more  particularly  to  the  production  of  sensory  phenomena,  where 
a  comparatively  small  visceral  lesion  gives  rise  to  an  irritable  focus  in  the 
spinal  cord,  and  to  extensive  suffering  and  widespread  areas  of  hyperalgesia, 
or  to  certain  mental  states  where  the  patients  sometimes  become  '  nervous  ' 
and  apprehensive.     The  result  of  the  association  of  heart  affections  with 


56  DISEASES  OF  THE  HEART 

these  latter,  may  be  summed  up  in  the  expression  that  the  cardiopath 
tends  to  become  a  neuropath. 

This  mental  state  is  seen  very  characteristically  in  both  men  and  women. 
If  they  have  been  told  that  they  have  a  murmur,  or  an  irregular  heart, 
or  if  they  are  conscious  of  an  extra-systole,  or  suffer  actual  distress  of 
a  cardiac  origin,  they  become  extremely  apprehensive.  The  hyperalgesia, 
so  common  in  the  breasts  of  women  suffering  from  some  slight  heart  trouble, 
is  a  constant  source  of  worry,  and  some  are  continually  imagining  that 
the  abnormal  soreness  is  an  indication  of  serious  disease.  This  apprehension 
is  unfortunately  too  often  aggravated  by  the  warnings  of  the  physician, 
who  estimates  the  significance  of  the  symptoms  too  seriously,  or  will  neither 
admit  nor  deny  the  gravity  of  the  condition. 

The  combination  of  cardiac  and  nervous  exhaustion  may  be  brought 
about  in  another  way.  People  with  a  tendency  to  '  nervous  debility  ',  or 
who  have  acquired  it  from  some  other  cause,  may  develop  some  cardiac 
trouble,  functional  or  organic.  In  such  people,  the  reflex  symptoms  are 
greatly  exaggerated.  Thus  one  of  my  patients  with  aortic  and  mitral 
disease  experienced  no  sensory  phenomena  until  she  developed  a  gastric 
ulcer.  This  gave  rise  to  great  pain,  and  to  a  widespread  area  of  hyper- 
algesia of  the  skin  and  muscles  in  the  left  side  of  the  abdomen.  Soon  after 
this  she  began  to  suffer  from  pain  from  the  heart  affection,  and  the  hyper- 
algesia finally  embraced  nearly  the  whole  of  the  left  chest.  The  patient 
lived  for  many  years  after  the  appearance  of  these  symptoms,  and  a  pyloric 
ulcer  and  aortic  and  mitral  valve  disease  were  found  on  post-mortem 
examination. 

In  all  these  cases  we  must  exercise  a  great  deal  of  judgement.  It 
frequently  happens  that  in  patients  with  a  demonstrable  cardiac  lesion, 
the  symptoms  are  estimated  too  seriously,  and  the  case  looked  upon  with 
greater  gravity  than  need  be.  On  the  other  hand,  if  there  be  no  murmur 
or  irregularity,  the  case  is  liable  to  be  treated  Ughtly  as  one  of  '  pseudo- 
angina  pectoris  '  or  neurasthenia. 

§  60.  Pseudo-angina  pectoris,  a  useless  and  misleading  term. — 
It  is  time  the  term  '  pseudo-angina  pectoris  '  was  dropped  out  of  medical 
literature.  While  it  may  be  convenient  to  group  under  indefinite  terms 
many  conditions  of  whose  nature  we  are  ignorant,  it  should  be  borne  in  mind 
that  this  grouping  is  but  provisional,  and  a  confession  of  our  ignorance 
of  the  real  nature  of  the  complaint.  With  advance  in  our  knowledge,  first 
one  complaint  and  then  another  should  be  placed  in  a  group  whose  cause 
is  definite  and  known.  In  this  way  many  cardiac  terms,  such  as  tachy- 
cardia, cmbryocardia,  bradycardia,  have  been  employed  loosely,  and  noAv 


HYPERSENSITIVE  NERVOUS  SYSTEM  57 

should  never  be  employed  unless  a  definition  be  given  of  what  is 
meant. 

The  term  '  angina  pectoris  '  is  employed  to  designate  a  group  of  sjnoaptoms 
evoked  by  the  heart,  of  which  pain  is  the  most  distinctive.  As  angina  pec- 
toris is  sometimes  associated  with  grave  organic  lesions,  we  find  such  cases 
referred  to  as  '  angina  pectoris  vera  '.  The  term  '  pseudo-angina  pectoris  ' 
is  applied  to  cases  in  which  the  pain  resembles  that  of  angina  pectoris  vera, 
but  is  due  to  some  other  cause  than  heart  disease,  or  in  Avhich  the  pain  arises 
from  the  heart  with  no  organic  lesion.  In  regard  to  the  former  class,  if  the 
pain  is  due  to  some  other  viscus,  e.g.  the  stomach,  as  sometimes  happens, 
why  call  it  '  pseudo-angina  pectoris  '  ?  If  it  is  due  to  the  stomach,  why  not 
say  so  ?  In  regard  to  the  latter  class,  the  employment  of  this  term  is  due 
to  a  total  misconception  of  the  nature  and  mechanism  of  visceral  pain. 
The  fundamental  cause  of  the  pain  is  the  same  in  the  case  of  the  heart  as 
in  that  of  any  other  viscus,  and  the  pain  is  as  readily  induced  in  the  heart 
as  in  the  stomach.  As  we  would  never  dream  of  calhng  a  stomach  pain 
a  '  pseudo-gastralgia  ',  so  we  need  not  call  a  heart  pain  '  pseudo-angina  '. 

I  deal  with  the  matter  at  length,  as  the  employment  of  a  fine-sounding 
term  has  too  often  sufficed  for  a  diagnosis,  so  that  no  inquiry  into  the  real 
nature  of  these  symptoms  has  been  undertaken.  In  the  great  majority  of 
cases  when  a  patient  complains  of  a  pain  in  his  chest  which  radiates  into  his 
arm,  in  the  area  shaded  in  Fig.  12  (p.  51),  the  pain  is  of  cardiac  origin.  The 
only  other  conditions  in  which  I  have  found  pain  to  occupy  this  characteristic 
site,  was  in  herpes  zoster  affecting  the  upper  dorsal  nerves  and  certain 
rare  forms  of  gastric  spasm.  In  one  case,  I  thought  I  had  to  deal  with 
a  case  of  angina  pectoris  until  the  herpetic  eruption  revealed  the  true  nature 
of  the  complaint.  It  is  quite  conceivable  that  other  conditions  may  give 
rise  to  pain  having  this  distribution,  but  that  is  no  reason  for  calling  them 
pseudo-angina  pectoris. 

The  characteristic  distribution  of  the  pain  and  other  sensory  phenomena 
at  once  excludes  hysteria,  for  in  the  latter  the  symptoms  do  not  follow  the 
anatomical  distribution  of  nerves.  When  a  hysterical  patient  feels  a  pain 
in  this  region,  it  may  be  assumed  that  there  is  probably  some  cardiac  trouble 
in  addition  to  the  hysteria. 

§  6i.  Exaggerated  sensory  phenomena  with  and  without  valvular 
disease — A  great  many  people  with  a  demonstrable  cardiac  lesion,  as  of 
the  aortic  or  mitral  valves,  develop  sensory  phenomena  in  an  exaggerated 
form.  This  is  particularly  seen  in  some  women  in  whom  the  reserve  force 
is  exhausted.  Such  folks  may  struggle  on  for  a  long  time,  working  hard 
and  ignoring  their  earlier  symptoms  of  a  limitation  of  the  field  of  cardiac 


58  DISEASES  OF  THE  HEART 

response,  determined  not  to  give  in.  Finally  the  nervous  system  shares  in 
the  exhaustion,  and  the  breakdown  is  brought  about  with  an  extreme 
development  of  the  sensory  phenomena  ;  thus  attacks  of  pain,  sometimes 
of  great  severity,  may  be  felt  across  the  chest  and  extending  into  the  left 
arm,  or  more  often  the  complaint  may  be  of  a  dull  aching  pain  of  varying 
severity,  but  distinctly  worse  at  the  end  of  a  day's  work.  The  hyperalgesia 
may  spread  over  a  very  extensive  area,  and  sometimes  is  extremely  acute. 

On  account  of  the  manifest  lesion  in  the  heart  these  cases  are  not  un- 
frequently  diagnosed  as  cases  of  angina  pectoris  of  a  severe  and  dangerous 
form,  and  I  have  known  them  lead  a  life  of  great  restriction  for  many  years 
under  this  mistaken  notion.  The  attacks  are  indeed  those  of  angina  pectoris, 
but  are  not  dangerous,  and  are  an  evidence  of  exhausted  heart  muscle, 
and  disappear  with  the  restoration  of  the  reserve  force. 

On  the  other  hand,  we  have  mothers  of  families  with  no  heart  murmurs, 
who  for  many  years  have  worked  hard  from  morning  till  night,  whose  sleep 
has  been  disturbed  by  ailing  or  fretful  children,  and  who  finally  break 
down  with  exhausted  heart  and  nervous  system.  Some  of  my  most  typical 
cases  have  been  in  young  women  whose  sleep  has  been  disturbed  frequently 
every  night  for  many  years  to  attend  to  an  ailing  parent.  This  constant 
strain  night  and  day  exhausts  the  strength.  These  patients  suffer  from 
heart  pain,  sometimes  with  the  classical  symptoms  of  angina  pectoris 
described  in  Chapter  VII. 

With  suitable  management  they  eventually  recover,  though  recovery 
is  usually  very  protracted,  the  patients  sometimes  having  to  lead  very  quiet 
lives  for  months  or  even  years.  Similar  symptoms  may  arise  in  others 
who  have  been  exposed  to  worry  and  anxiety,  or  who  have  suffered  from 
sleeplessness,  while  others  may  suffer  when  there  is  no  apparent  reason  for 
the  exhaustion. 

§  62.  Exaggerated  sensory  phenomena  in  early  cardio-sclerosis. — 
The  possibility  that  in  these  cases  there  may  be  beginning  cardio-sclerosis, 
should  be  kept  in  mind,  especially  in  cases  over  40  years  of  age.  There  is 
nothing  to  tell  whether  it  is  so  or  not,  for  the  superficial  arteries  may  be  quite 
normal  in  appearance,  and  the  blood-pressure  give  no  sure  information.  This 
needs  to  be  specially  insisted  on  when  these  exaggerated  phenomena  appear 
in  women  between  50  and  60.  I  have  seen  a  number  of  patients  develop 
all  the  sensory  phenomena  in  an  extremely  exaggerated  form,  becoming 
weaker  until  they  were  unable  to  leave  their  beds  ;  some  have  become 
unconscious,  and  died  ;  others  regained  consciousness,  and  after  a  time 
sufficient  strength  to  go  about  for  years.  After  their  recovery  I  have  been 
surprised  to  find  an  aortic  systolic  murmur,  which  had  not  been  present 


HYPERSENSITIVE  NERVOUS  SYSTEM  59 

prior  to  the  breakdown.  Some  of  these  have  remained  liable  to  attacks 
of  angina  ;  one  dropped  down  dead,  and  in  another,  who  died  from  sub- 
sequent heart  failure,  there  was  marked  sclerosis  of  the  heart  muscle, 
coronary  arteries,  aortic  valves,  and  aorta.  The  diagnosis  in  these  cases 
depends  on  the  response  to  treatment  (§  57). 

§  6^.  Characteristics  of  the  sensory  phenomena.  — There  are  some 
special  points  in  these  cases  that  distinguish  them  from  those  who  do  not 
have  the  same  susceptible  nervous  system.  The  suffering  may  not  be  as 
severe  as  in  the  more  grave  forms  of  angina  pectoris,  but  it  is  more  lasting 
and  comes  on  after  periods  of  continuous  exertion.  Sometimes  it  is  limited 
to  the  left  arm,  if  that  arm  has  been  much  employed  in  work,  as  in  washing 
or  baking.  It  is  frequently  associated  with  extreme  tenderness  on  pressure 
of  the  tissues  of  the  left  chest  and  neck,  especially  the  left  breast,  the  pecto- 
ralis  major  and  sterno-mastoid  muscles.  After  testing  the  tender  skin  and 
muscles  by  slightly  pinching  the  skin  and  muscles  between  the  fingers  and 
thumb,  the  part  becomes  extremely  sore,  and  the  aching  lasts  for  hours 
afterwards.  When  the  patient  is  suffering  from  severe  pain,  the  mouth  may 
become  dry  and  parched,  and  large  quantities  of  pale  urine  may  be  passed, 
as  happens  in  cases  where  the  angina  pectoris  is  of  very  grave  significance. 

§  64.  Air  suction — Another  symptom  is  extremely  common  in  these 
cases — the  belching  of  air.  One  searches  textbooks  in  vain  for  any  hint 
as  to  the  nature  of  this  symptom,  and  though  it  is  extremely  common  in 
all  neurotic  people,  its  significance  is  almost  invariably  misunderstood. 
A  detailed  and  satisfactory  account  is  given  by  Wyllie,**^  and  it  is  to  this 
article  I  owe  enlightenment  as  to  the  meaning  of  this  symptom. 

The  chief  feature  is  the  noisy  expulsion  of  air  from  the  stomach.  Patients 
complain  of  attacks  of  flatulence,  and  in  these  attacks  seemingly  expel 
large  quantities  of  air,  but  if  closely  watched  they  will  be  seen  first  to  suck 
air  into  their  stomachs.  Before  expelling  the  air,  they  unconsciously  close 
the  glottis,  fix  the  muscles  of  the  abdominal  wall,  then  expand  the  chest. 
As  no  air  goes  into  the  lungs,  and  the  diaphragm  is  raised,  the  pressure  in 
the  stomach  becomes  negative.  By  this  process  they  suck  air  into  the 
stomach.  After  sucking  in  a  quantity,  they  expel  it  with  considerable 
force,  and  often  with  a  good  deal  of  noise.  Many  people  can  do  this  at 
will,  others  only  in  certain  states  of  excitement.  Some  have  '  attacks  of 
flatulence '  in  the  middle  of  the  night,  and  such  attacks  are  due  to  air 
swallowing,  or  more  correctly  air  suction.  As  Wyllie  points  out,  these 
attacks  can  be  stopped  by  making  the  patient  open  his  mouth  widely,  and 
keeping  the  jaw  propped  open  by  a  large  cork  between  the  teeth,  a  procedure 
which  prevents  the  air  suction. 


60  DISEASES  OF  THE  HEART 

I  have  watched  several  patients  during  an  attack  of  angina  pectoris, 
and  when  they  stand  seemingly  immobile,  they  unconsciously  suck  air  into 
the  stomach.  Immediately  the  pain  subsides  the  air  is  expelled,  and  the 
patient  is  apt  to  attribute  the  relief  he  has  experienced  to  the  coincident 
and  demonstrable  act.  This  very  obvious  phenomenon  has  led  many 
observers  to  imagine  that  the  attack  was  gastric  in  origin,  and  hence  the 
group  of  gastric  '  pseudo-anginas  '. 

This  association  of  air  suction  with  attacks  of  angina  pectoris,  which 
is  sometimes  found  in  men,  is  extremely  common  in  women.  As  air  suction 
is  frequent  in  women,  it  is  sometimes  mistaken  for  a  hysterical  symptom, 
and  its  relationship  to  a  real  heart  attack  is  apt  to  be  overlooked.  As 
a  matter  of  fact,  attacks  of  air  suction  are  apt  to  arise  from  any  exciting 
cause,  and  attacks  of  angina  pectoris  readily  induce  them.  In  some  it 
occurs  so  readily  that  it  may  come  on  before  the  real  suffering.  Thus,  one 
lady  who  suffered  from  extreme  arterial  degeneration,  had  severe  attacks  of 
angina  pectoris,  which  disappeared  after  a  long  period  of  rest  in  bed. 
When  she  got  about  again,  she  could  walk  on  the  level  with  comfort,  but 
the  slightest  hiU  brought  on  discomfort,  which  if  not  heeded  resulted  in  great 
pain  in  the  chest.  As  a  rule,  however,  before  the  pain  became  severe  she 
began  to  suck  in  and  to  expel  air.  She  would  rest  a  minute  and  start  again, 
but  soon  had  to  stop,  and  expel '  more  wind  '  as  she  put  it. 

§  65.  The  circulatory  symptoms  in  the  X  disease.* — There  is  another 
class  of  cases  of  somewhat  indefinite  character,  that  needs  to  be  recognized 
in  order  to  appreciate  other  forms  of  heart  trouble.  The  class  I  allude  to 
will  be  recognized  by  every  practitioner  as  they  form  a  considerable  portion 
of  the  community.  The  individual  is  spare  and  thin  ;  the  face  is  often 
drawn  and  lined,  sometimes  even  in  the  young.  It  is  usually  pale,  though 
in  some  the  face  is  ruddy,  and  the  nose  is  red  in  cold  weather.  The  hands 
are  usually  cold,  and  they  teU  you  their  circulation  is  feeble.  They  are 
always  worse  on  raw  cold  days,  and  feel  chilly  and  ill  after  a  cold  bath. 
Their  complaints  are  extremely  varied,  and  many  have  a  fixed  idea  that 
certain  organs  are  at  fault,  and  it  is  true  that  some  trouble,  usually  slight, 
may  be  found  in  some  organ.  Thus  we  find  gastric  and  bowel  complaints 
extremely  common,  though  other  viscera  may  also  be  at  fault  and  com- 

*  I  employ  the  term  '  X  disease  '  for  the  reason  that  I  do  not  know  the  nature  of  this  com- 
plaint. Many  physicians  call  members  of  this  class  '  neurasthenics  ',  and  are  content  to  leave 
the  matter  there.  This  is  simply  to  give  a  complaint  a  name,  which  is  so  satisfying  that  the 
fact  is  often  lost  sight  of  that  the  name  sheds  no  light  upon  the  complaint  and  is  nothing  but 
a  cloak  for  ignorance.  If  the  term  '  X  disease  '  be  employed  it  will  be  a  glaring  acknowledgement 
of  our  ignorance,  and  will  lead  to  a  constant  endeavour  to  clear  up  the  mystery  surrounding 
these  cases. 


HYPERSENSITIVE  NERVOUS  SYSTEM  61 

plained  of.  The  patient's  mental  condition  is  curious  and  interesting. 
Some  of  them  are  sane,  level-headed,  and  extremely  intelligent.  To  these 
the  bodily  suffering  is  nothing  more  than  a  grievous  and  troublesome 
affliction.  In  others  it  leads  to  irritability  and  peevishness  in  temper. 
Some  become  introspective,  and  are  deeply  concerned  about  their  bodily 
or  spiritual  affairs.  It  alters  their  views  of  material  things  ;  cranks  and 
faddists,  political,  religious,  and  dietetic,  are  common  among  them,  often 
exhibiting  strenuous  enthusiasm  for  their  particular  ideas.  Another  aston- 
ishing feature  in  these  cases  is  the  remarkable  way  in  which  a  temporary 
recovery  may  take  place.  For  weeks  some  of  these  folks  may  go  about 
miserable  and  ill,  taking  little  food,  finding  that  little  too  much  for  the 
digestion,  and  searching  for  some  kind  that  will  suit  them — when  suddenly 
they  feel  better.  Their  recovery  may  last  for  weeks  or  even  months,  but 
they  generally  relapse. 

Now  this  peculiarity  leads  to  another  characteristic  of  this  complaint — 
unbounded  and  unreasoning  belief  in  what  they,  take  to  be  the  cause  of 
their  recovery,  diet,  drug,  methods  c^  exercise,  operation.  It  is  because 
of  this  tendency  to  recover  that  there  are  so  many  cures.  If  one  reads 
between  the  lines  of  the  testimonials  in  favour  of  certain  remedies,  empiric 
or  recognized  by  authority,  we  can  see  that  it  is  this  class  of  case  that  is 
being  treated.  It  is  especially  among  them  that  faith-cures  abound,  and 
these  are  the  people  who  swell  the  ranks  of  Christian  Scientists.  Emotional 
excitement,  whether  of  love  or  religion,  always  relieves  this  kind  of  person, 
and  so  when  religion  comes  into  play  we  get  the  various  forms  of  faith- 
healing.     Many  women  feel  extremely  well  when  pregnant. 

The  diagnoses  of  medical  men  are  as  numerous  and  varied  as  the  com-/ 
'plaints  of  the  patient.  The  gynaecologist  diagnoses  some  pelvic  disorder  ;/ 
jthe  surgeon  sees  the  source  of  all  the  trouble  in  an  appendix,  a  dilated 
stomach,  or  a  wandering  kidney  ;  while  the  physician  recognizes  the  disease 
according  to  the  bent  of  his  studies — a  heart  affection,  visceral  stasis,  gastro- 
ptosis,  neurasthenia,  atonic  dyspepsia,  and  so  forth.  So  minute  indeed 
!  are  some  of  the  diagnoses,  that  we  find  them  classified  further  as  cardiac, 
gastric,  mental,  or  renal  neurasthenias. 

I  enter  into  the  description  of  this  class  of  case  somewhat  fully  because 
many  of  them  masquerade  as  cases  of  heart  disease.  I  have  for  some  years 
been  inquiring  into  the  nature  of  the  symptoms  in  these  cases,  and  here  detail 
some  of  the  cardio- vascular  phenomena,  as  the  lack  of  the  recognition  of 
the  nature  of  these  symptoms  often  leads  to  a  mistaken  diagnosis. 

The  most  outstanding  feature  is  cold  hands,  and  this  is  sometimes  asso- 
ciated with  a  peculiar  roughness  and  thickness  of  the  skin.     The  fingers  may 


62  DISEASES  OF  THE  HEART 

become  white  and  numb  ;  '  dead  '  is  the  term  often  appHed.  Exposure 
on  a  very  cold  day  may  cause  the  condition  to  be  so  extreme  that  pain  in 
the  finger  ends  is  very  severe,  and  in  one  case  I  have  seen  a  shght  gangrene 
follow.  The  nose  is  often  red,  and  the  association  between  dyspepsia  and 
the  red  nose  is  extremely  common  in  these  folks.  There  is  very  often  dilata- 
tion of  the  stomach,  associated  with  accumulation  of  blood  in  the  abdomina 
veins.  This  latter  can  be  demonstrated  in  several  interesting  ways.  If  the 
patient  be  laid  on  his  back,  and  very  gentle  pressure  be  steadily  appUed  with 
the  hands  placed  on  the  upper  part  of  the  abdomen,  so  as  not  to  interfere 
with  the  respiration,  the  veins  of  the  neck  will  gradually  be  seen  to  swell 
and  the  pulsation  in  them  becomes  greatly  increased.  In  some  cases  this  may 
be  seen  to  occur  during  quiet  respiration,  the  swelling  of  the  vein  occurring 
during  inspiration.  The  cause  of  the  swelling  in  this  condition  is  that 
pressure  on  the  abdomen  empties  the  abdominal  veins  into  the  right  heart,  so 
that  there  is  less  accommodation  for  the  blood  returning  by  the  superior 
vena  cava  ;  hence  the  jugular  vein  distends.  Inspiration  causing  a  descent 
of  the  diaphragm  compresses  the  abdominal  contents,  including  the  large 
veins,  against  the  unjdelding  waU,  and  brings  about  the  same  result. 
G.  Oliver  says  that  by  putting  a  bag  of  shot  (14  lb.)  on  the  abdomen  in 
these  cases  he  can  raise  the  pressure  in  the  arterial  system. 

The  heart  itself  in  these  cases  is  sometimes  sUghtly  dilated,  and  there 
may  be  mitral  and  tricuspid  systolic  murmurs.  They  are  very  evanescent, 
present  at  one  minute  and  gone  the  next.  Sometimes  we  can  detect  them 
at  the  beginning  of  an  examination,  and  in  a  few  minutes  they  have  dis- 
appeared. The  rate  and  rhythm  of  the  heart  often  varies.  Sometimes 
it  is  rather  slow,  and  sometimes  it  is  irregular,  the  irregularity  usually 
being  respiratory,  though  occasionally  extra-systoles  are  present,  and  then 
the  patient  if  conscious  of  them  is  often  greatly  frightened,  particularly 
if  the  doctor  does  not  convincingly  reassure  him.  Hesitation  or  doubt  on 
the  part  of  the  doctor  hangs  like  a  cloud  over  the  patient. 

I  have  been  particularly  struck  with  the  slow  respiration  in  a  number  of 
these  cases.  It  may  faU  as  low  as  seven  per  minute  (Fig.  77,  Plate  II),  and  the 
patient  be  free  from  any  distress,  and  quite  unconscious  that  anything  is 
wrong.  It  is  then  that  the  heart  rhythm  is  most  affected,  and  the  swelling 
of  the  vein  during  inspiration  and  from  pressure  on  the  abdomen  occurs 
most  characteristically.  The  nature  of  this  irregularity  is  fully  described 
in  Chapter  XVIII.  A  healthy  individual  can  sometimes  produce  this 
irregularity  by  simply  breathing  slowly  and  deeply  at  the  rate  of  seven  or 
eight  per  minute. 

§  66.  Vaso-motor  angina  pectoris — For  many  years  I  was  at  a  loss 


HYPERSENSITIVE  NERVOUS  SYSTEM  63 

to  understand  the  cases  described  by  Nothnagel  ^^  as  vaso-motor  angina 
pectoris.  The  term  is  such  a  fine-sounding  one  that  it  soon  found  its  way 
into  current  literature,  but  I  could  never  find  it  employed  in  the  sense 
in  which  Nothnagel  used  it,  nor  did  the  cases  recorded  by  others  correspond 
with  those  given  by  him.  I  have  come  across  several  patients  who  suffered 
from  angina  pectoris,  and  a  careful  scrutiny  of  their  symptoms  leads  me 
to  think  that  these  are  the  kind  of  patient  described  by  Nothnagel.  They 
are  particularly  liable  to  cold  and  chilly  attacks.  Occasionally  the  attacks 
of  chilliness  persist,  and,  if  the  patients  have  no  opportunity  to  warm 
themselves,  increase  in  intensity,  until  after  an  hour  or  two  of  misery  they 
culminate  in  attacks  of  pain  in  the  chest,  radiating  into  the  arm.  The 
pain  in  severe  cases  persists  with  varying  intensity  until  the  patient  gets 
thoroughly  warmed. 

I  deal  particularly  with  this  subject  because  the  term  '  vaso-motor  angina 
pectoris  '  conveys  to  many  minds  some  definite  idea  of  what  happens  in  these 
cases,  and  though  I  can  formulate  no  explanation  that  would,  to  my  mind, 
satisfactorily  explain  the  matter,  I  may  point  out  that  in  these  cases,  the 
blood-pressure  is  not  increased  as  one  would  expect,  if  the  explanation  were 
merely  that  the  heart  is  acting  against  increased  peripheral  resistance. 
Although  I  have  not  taken  the  blood-pressure  during  a  severe  attack  of  pain, 
I  have  taken  it  in  a  number  of  cases  when  the  extremities  were  cold  and 
chilly  and  the  patient  suffering  considerable  distress,  and  the  pressure  has 
invariably  been  low — about  120-130  mm.  Hg. 

§  67.  Prognosis  in  cases  with  exaggerated  sensory  symptoms If 

care  be  taken  to  differentiate  between  the  patients  who  exhibit  exaggerated 
nervous  phenomena  due  to  progressive  organic  lesions,  and  those  due  to 
exhaustion  apart  from  a  progressive  lesion,  the  prognosis  can  be  made  with 
fair  certainty.  Recovery  almost  invariably  results  in  the  latter  class, 
though  it  may  be  delayed  for  a  long  time.  Naturally,  the  compHcation 
producing  the  nerve  exhaustion  must  be  taken  into  account,  and  if  due  to 
other  visceral  affections,  the  prognosis  depends  also  upon  their  nature. 

When  there  is  an  organic  lesion,  as  cardio-sclerosis,  or  valvular  disease, 
on  the  whole  the  exaggerated  nervous  phenomena  do  not  add  to  the 
gravity,  but,  it  has  even  seemed  to  me,  act  favourably  in  many  cases, 
for  the  early  exhaustion  is  attended  by  such  an  amount  of  suffering,  that  the 
heart  is  protected  from  more  extensive  exhaustion  of  its  reserve  force. 

In  the  cases  included  in  the  groups  of  X  disease,  even  when  angina 
pectoris  is  present,  I  have  never  found  the  heart  trouble  give  rise  to  a 
serious  breakdown,  nor  have  I  ever  found  death  from  heart  failure  in  this 
type  of  patient.     In  fact,  they  are  among  the  long-lived,  for  they  usually 


64  DISEASES  OF  THE  HEART 

take  such  care  of  themselves  that  they  avoid  all  risks  and  exposure  to 
danger. 

§  68.  Treatment. — It  is  of  the  first  importance  that  we  should  appre- 
ciate the  nature  of  the  trouble  in  these  cases,  and  bear  in  mind  the  part  played 
by  the  nervous  system.  The  nervous  element  is  often  the  chief  one  to 
be  considered,  and  the  sufferings  of  many  of  these  patients  are  aggravated 
by  the  consciousness  or  dread  of  some  serious  affection  of  the  heart.  Having 
satisfied  ourselves  as  to  the  real  nature  of  the  trouble,  we  should  first  of  aU 
reassure  the  patient.  In  a  great  many  cases  success  in  treatment  depends 
on  this,  and  we  can  often  see  patients  at  once  made  well,  or  greatly  improved, 
when  they  become  fully  reassured.  This  is  more  particularly  the  case  when 
the  patient  has  previously  been  alarmed  by  being  told  that  the  condition 
was  serious.  The  peculiar  mental  factor  that  makes  this  class  of  patient 
the  stay  and  support  of  many  forms  of  empirical  or  semi-empirical  treatment, 
should  be  kept  in  mind.  As  suggestion  plays  an  important  part  in  the 
numerous  special  methods  of  cure,  it  should  be  used  inteUigently  by  medical 
men,  and  in  a  legitimate  manner,  that  is  to  say,  the  patient  should  be 
reassured  from  the  standpoint  of  a  full  knowledge  of  his  condition. 

There  is  a  great  tendency  for  the  physician  to  attach  too  high  an  im- 
portance to  a  case  with  exaggerated  nervous  symptoms,  where  there  is  an 
organic  lesion  of  the  valves.  I  have  seen  many  patients  lead  fives  of  great 
restriction,  with  a  certain  amount  of  fear,  on  account  of  the  supposed  serious- 
ness of  heart  trouble.  Women  have  had  attacks  of  angina  pectoris,  and 
have  been  forbidden  to  undertake  their  household  duties.  Great  numbers 
have  gone  to  health  resorts  at  great  expense  and  inconvenience  year  after 
year,  to  perform  the  '  cure  ',  because  in  their  days  of  suffering  they  had 
experienced  benefit.  When  there  is  a  valvular  murmur,  we  must  carefully 
inquire  into  the  conditions  that  have  induced  the  heart  exhaustion  and  the 
attendant  suffering,  and  consideration  of  the  whole  of  the  facts  wiU  enable 
us  with  certainty  to  recognize  the  real  nature  of  the  phenomena.  We 
can  often  with  certainty  reassure  the  patient  that  with  suitable  treatment 
the  suffering  will,  to  a  great  extent,  disappear,  and  that  though  the  organic 
trouble  may  persist,  with  intelligent  management  there  is  good  ground 
for  hope  of  a  fair  restoration  to  health.  In  many  cases  one  is  able  to  do  more, 
to  point  out  that  the  suffering  is  a  safeguard,  its  first  appearance  being  an 
evidence  that  the  patient  is  exhausting  the  reserve  force  of  the  heart,  and 
that  such  restrictions  are  necessary  to  guard  against  further  exhaustion. 

This  inteUigent  appreciation  of  symptoms  is  of  service  in  other  ways. 
Thus,  when  patients  become  conscious  of  an  extra-systole,  they  are  often 
subjected  to  long  courses  of  treatment,  usually  inefficient,  by  their  medical 


HYPERSENSITIVE  NERVOUS  SYSTEM  65 

attendant,  or  by  some  special  method.  The  mere  reassurance  of  the  harm- 
lessness  of  the  symptoms  would  have  done  more  good  than  all  the  treatment. 
As  an  illustration  I  cite  the  following  experience.  A  professional  football- 
player  consulted  me  because  his  heart  '  stopped  '  at  times.  He  had  been 
seen  by  two  doctors,  who  forbade  him  to  play,  and  put  him  on  digitalis  and 
strychnine.  This  cessation  of  work  was  a  serious  matter  to  him,  because 
if  he  could  not  complete  his  engagement  for  the  season  he  lost  the  chance 
of  a  benefit  match,  which  he  looked  upon  as  a  reward  at  the  end  of  his  services 
as  a  footballer.  Except  that  he  was  frightened  and  nervous  I  found  him 
in  all  respects  a  healthy  man,  save  for  a  somewhat  frequent  extra-systole. 
I  told  him  he  could  start  playing  at  once,  and  that  when  he  was  conscious 
of  his  heart  stopping  he  was  to  pay  no  attention  to  it.  He  at  once  resumed 
his  engagements  and  completed  his  term  with  no  discomfort.  He  told  me 
that  at  the  beginning  of  one  match  he  was  painfully  conscious  of  his  heart's 
irregularity,  and  felt  he  must  retire,  but  reflected  upon  what  I  had  told  him, 
dashed  into  the  game,  and  in  a  few  minutes  forgot  aU  about  his  trouble,  and 
said  he  never  played  better  in  his  life. 

I  use  this  illustration  to  emphasize  the  fact  that  neither  the  exaggerated 
sensory  and  mental  sensations,  nor  the  symptoms  giving  rise  to  them,  should 
be  the  guide,  but  what  effort  the  heart  can  undertake  without  discomfort. 

Besides  reassuring  the  patient,  steps  should  be  made  to  remove  him  or 
her  from  any  conditions  that  conduce  to  the  exhaustion,  such  as  over- 
work, worry,  nursing  a  sick  relative.  Discretion  must  be  used,  and  the 
patient's  circumstances  considered.  When  the  patients  are  well-to-do,  a 
complete  change  in  the  mode  of  life  is  often  very  efficacious,  and  they  may 
be  sent  away,  the  choice  of  the  place  depending  on  the  patient's  tastes.  If 
they  can  undergo  some  physical  effort,  a  holiday  may  be  recommended  that 
includes  some  exertion,  such  as  hill-climbing,  cycling,  golfing,  or  '  sight- 
seeing ' — town  or  country — ^provided  the  occupation  interests  the  patient. 
They  may  be  sent  to  some  watering-place,  and  may  indulge  in  the 
special  treatment  adopted  there — for  the  sake  of  doing  something,  and 
getting  what  benefit  hydrotherapy  may  convey.  My  patients  have  gone 
to  all  sorts  of  places,  and  those  who  went  to  the  seaside  and  indulged  in 
sea-bathing  got  more  benefit  than  those  who  frequented  the  more  vaunted 
inland  spas,  home  or  continental.  The  fife  there  is  more  bracing,  and  there 
is  less  opportunity  to  meet  all  sorts  of  neurotics,  and  the  baneful  habit  of 
comparing  experiences  is  thus  not  so  easy  to  indulge  in. 

The  vast  majority  of  patients  cannot  go  away  and  leave  their  posts,  and 
these  form  the  class  with  which  the  general  practitioner  has  often  a  great 
deal  of  trouble.     With  patience  and  perseverance,  however,  much  can  be 

MACKEXZIE  -ci 


66  DISEASES  OF  THE  HEART 

done  for  them,  and  in  many  instances  the  doctor  can  give  great  help  to  some 
of  the  most  deserving  patients  he  has  to  treat.  The  mother  of  a  family  has 
to  keep  going,  the  tired  daughter  has  to  nurse  the  aiUng  parent.  In  all 
these  cases  there  will  be  found,  almost  invariably,  insufficient  sleep,  or  sleep 
frequently  disturbed,  and  this  is  often  the  real  cause  of  the  trouble  and 
in  addition  renders  the  patient  peevish  and  irritable.  Much  can  be  done 
by  suggesting  different  devices  to  promote  the  patient's  rest.  In  many  cases 
we  have  to  resort  to  drugs,  and  happily  the  most  efficacious  hypnotic  in 
these  cases  is  also  the  safest,  namely,  bromides  (particularly  bromide  of 
ammonium),  which  should  be  given  until  the  patient  sleeps  soundly.  Often 
they  produce  drowsiness  and  languor  during  the  day,  and  the  patient  may 
complain  of  being  weaker  than  ever.  This  is  no  contra-indication,  but  the 
contrary,  for  the  languor  induces  idleness  and  restfulness.  She  does  less 
work,  she  is  less  irritable,  and  the  heart  is  not  so  easily  excited.  After  a 
few  weeks,  if  the  dose  be  gradually  diminished,  it  will  often  be  found  that 
in  the  meantime  the  patient's  condition  has  wonderfully  improved.  The 
necessity  of  continuing  her  duties  prevents  the  possibility  of  any  immediate 
recovery,  but  by  the  judicious  administration  of  the  bromides,  patients 
can  be  tided  over  trying  periods  for  months  or  years. 

'  Heart  tonics  '  in  these  cases  are  of  little  use.  Even  if  they  had  the  action 
they  are  supposed  to  possess,  it  is  doubtful  if  their  administration  would  be 
wise.     It  is  not  a  whip  an  overworked  horse  needs,  but  rest. 

The  nourishment  of  the  patient  often  leaves  much  to  be  desired.  The 
household  duties  and  the  cooking  take  away  the  appetite,  and  they  content 
themselves  with  stuff  easily  swaUowed  and  stimulating — hot  fluids,  tea, 
coffee,  and  spirits.  The  food  should  be  taken  in  small  quantities  and  often, 
and  should  be  fairly  dry  to  ensure  slow  mastication.  It  is  sometimes  a  good 
plan  to  suggest  a  dietary  of  a  very  simple  nature.  Find  out  what  food  the 
patient  prefers,  and,  if  it  is  rational,  so  arrange  the  diet  that  every  few  hours 
may  bring  a  change,  even  if  it  be  but  an  egg  at  one  time,  and  a  dry  biscuit 
and  a  few  tablespoonfuls  of  milk  at  another.  In  all  cases  stimulants  should 
be  forbidden.  The  great  exhaustion  brought  about  by  the  long  weary  hours 
of  work  and  suffering  is  often  speedily  temporarily  relieved  by  spirits  ;  but 
these  are  just  the  people  who  ultimately  find  solace  in  increasing  quantities, 
until  the  habit  becomes  all  too  powerful. 


CHAPTER   IX 

INSTRU3IENTAL   METHODS    OF   EXAMINATION 

§  69.  The  sphygmograph. 

70.  The  polygraph. 

71.  The  clmical  polygraph. 

72.  The  ink  polygraph. 

In  the  examination  of  the  vast  majority  of  patients,  the  diagnosis  can 
be  made  independently  of  graphic  records.  It  must  not  be  inferred  from 
this  that  graphic  records  can  be  dispensed  Avith,  for  the  power  to  diagnose 
the  great  majority  of  cases  comes  through  the  information  obtained  by 
this  means.  Though  it  is  not  necessary  for  a  physician  himself  to  take 
records,  he  must  be  familiar  with  their  interpretation  in  order  that  he  may 
appreciate  and  apply  the  results. 

There  have  been  many  methods  devised  to  record  the  movements  of 
the  circulation,  but  here  I  will  only  deal  with  those  which  in  my  hands 
have  yielded  very  satisfactory  results.  The  essence  of  a  method  should  be 
simplicity,  for  the  more  complicated  the  processes  the  more  unsuitable 
it  becomes  for  practical  clinical  purposes.  In  hospitals  with  large  staffs 
of  assistants  the  more  elaborate  methods  may  be  usefully  employed,  but  for 
the  practitioner  who  studies  his  own  patients,  the  simpler  the  methods  the 
better. 

§  69.  The  sphygmograph. — It  is  scarcely  necessary  to  enter  into 
a  full  account  of  the  construction  of  the  various  sphygmographs.  They 
have  been  so  frequently  described  in  textbooks  that  their  construction  is 
famihar  to  all  medical  men.  They  are  all  practically  constructed  on  the 
same  principle.  A  steel  spring  is  laid  upon  the  radial  artery  at  the  wrist 
in  such  a  manner  that,  while  it  compresses  the  artery,  it  does  not  obliterate 
it.  Attached  directly  to  the  spring  is  a  long  lever,  or  a  series  of  small  levers, 
that  magnify  the  movements  of  the  spring.  The  free  extremity  of  the  lever 
presses  hghtly  against  a  strip  of  paper,  whose  surface  has  been  blackened 
by  the  smoke  of  burning  camphor  or  turpentine,  the  strip  of  paper  passing 
at  a  uniform  speed  by  means  of  a  clockwork  arrangement.  Although  I  have 
worked  with  several  instruments,  I  find  the  Dudgeon  to  be  the  handiest 
and  most  useful.     Into  all  sphygmographic  records,  certain  errors,  due  to 

F  2 


68  DISEASES  OF  THE  HEART 

defects  of  the  instruments,  creep.  Some  of  the  more  elaborate  instruments 
may  be  freer  from  defect  than  the  Dudgeon,  but  so  long  as  one  is  cautious 
not  to  read  itito  the  tracings  movements  evidently  due  to  instrumental 
errors,  the  Dudgeon  sphygmograph  is  quite  serviceable  for  a  great  many 
practical  purposes,  and  more  particularly  for  giving  a  true  and  accurate 
record  of  the  occurrence  of  pulse  beats. 

§  'JO.  The  polygraph. — There  are  many  perceptible  movements  due 
to  the  circulation  that  the  sphygmograph  fails  to  register,  and  when  it  is 
required  to  record  these  movements  other  instruments  have  to  be  employed. 
The  method  most  commonly  adopted  has  been  by  conveying,  by  means  of 
a  tube  containing  air,  the  movements  to  be  registered  to  a  tambour  on 
which  there  rested  a  lever.  The  excursion  of  the  lever  is  recorded  on  a 
revolving  drum  covered  by  smoked  paper.     Two  or  more  tambours  being 


B 

Fig.  13.    Shows  the  shallow  cups  or  '  receivers  '  used  in  taking  tracings  of  the  liver  (receiver  B) 
and  of  the  jugular  or  carotid  pulse  or  apex  beat  (receiver  E).     (Half  size.) 

used  with  their  levers  placed  one  above  the  other,  the  simultaneous  record 
of  different  movements  can  be  readily  effected. 

The  elaborate  and  bulky  apparatus  required  has  restricted  the  employ- 
ment of  this  method  to  such  narrow  limits,  that  numerous  points  of  interest 
in  chnical  medicine  have  been  either  overlooked  or  misunderstood.  In  my 
investigations  into  the  nature  of  the  venous  pulse,  I  had  at  first  to  use  this 
unwieldy  instrument,  but  its  cumbersomeness  compelled  me  to  devise 
a  much  simpler  and  more  effective  apparatus. 

§  71.  The  clinical  polygraph — This  apparatus,  which  I  have  called 
the  clinical  polygraph,  can  be  used  for  taking,  at  the  same  time  and  on  the 
same  recording  surface,  tracings  of  the  radial  pulse,  with  tracings  of  the 
apex  beat,  carotid,  venous,  or  liver  pulse,  or  the  respiratory  movements, 
and  its  size  permits  of  it  being  carried  about  with  the  greatest  facility,  and 
readily  employed  in  general  practice  (Fig.  14). 

The  essential  parts  of  the  instrument  are  a  small  cup  for  receiving  the 
impressions  of  the  pulsations,  a  tube  for  transmitting  the  impressions  to 


INSTRUMENTAL  METHODS  OF  EXAMINATION 


69 


a  tambour  and  lever,  the  tambour  being  attached  to  a  Dudgeon  or   Jacquet 
sphygmograph. 

The  smaU  cup  for  receiving  the  impressions  (which  will  be  referred  to 
hereafter  as  the  '  receiver  ')  is  simply  a  small  shallow  vessel,  circular  in  shape, 
one  and  a  half  inches  in  diameter  and  half  an  inch  in  depth  {E,  Figs.  13  and 
18).  The  open  mouth  is  applied  over  the  pulsating  part  so  that  its  edges  are 
closely  adapted  to  the  skin  and  all  communication  with  the  outer  air  is 
excluded.  From  the  roof  of  the  receiver  rises  a  narrow  pipe,  half  an  inch 
in  length.  To  this  pipe  is  fitted  an  india-rubber  tube  three  to  four  feet  in 
length,  the  other  end  of  which  is  connected  with  the  tambour.  A  modifi- 
cation of  this  receiver  is  required  when  tracings  of  the  liver  pulse  are  taken. 
The  '  liver  receiver  '  (B,  Fig.  13)  is  larger,  being  five  inches  in  length,  two 


Fig.  14.     The  clinical  polygraph,  consisting  of  a  tambour  attached  to 
a  Dudgeon's  sphygmograph. 


inches  in  breadth,  and  one  inch  in  depth,  its  open  edges  slightly  curved  on 
their  long  axis.  A  small  air-hole  is  made  at  one  end  near  the  roof.  In 
employing  the  '  liver  receiver  '  the  position  of  the  lower  margin  of  the  liver 
having  been  ascertained,  the  receiver,  held  in  the  right  hand,  is  laid  length- 
wise across  the  abdomen,  its  lower  edge  being  two  inches  below  the  liver 
margin,  and  the  end  with  the  air-hole  towards  the  middle  line.  Steady 
continuous  pressure  is  appUed  to  the  lower  margin  of  the  receiver  till  it 
presses  deeply  into  the  abdomen,  and  then  the  upper  margin  is  adapted 
closely  to  the  skin.  In  this  manner  a  considerable  portion  of  the  lower  liver 
edge  is  embraced  by  the  receiver.  If  the  forefinger  of  the  right  hand  is 
now  applied  over  the  air-hole,  the  movements  of  respiration  and  liver  pulse 
will  be  communicated  to  the  lever.  If  the  patient  stops  breathing,  the  liver 
movements  are  alone  transmitted. 

The  tambour  (Fig.  15)  supports  a  writing  lever  about  six  inches  in  length. 
From  the  under  surface  of  the  tambour  a  pipe  protrudes,  which  is  connected 


70 


DISEASES  OF  THE  HEART 


by  the  india-rubber  tubing  with  the  receiver.  Screwed  tightly  to  the  bottom 
of  the  tambour  is  a  stem  (B)  six  and  a  half  inches  in  length,  projecting  out- 
ward parallel  to  the  under  surface  of  the  tambour.  Half  an  inch  of  the  other 
extremity  of  the  stem  is  bent  almost  at  right  angles  (0),  and  this  portion 
fits  into  a  slot  on  the  upright  stem  that  supports  the  movable  lever  of  a 
Dudgeon's  sphygmograph  (Eig.  14).  Wlien  the  tambour  arrangement  is 
adjusted  to  the  sphygmograph,  the  tambour  rests  with  its  movable  surface 
vertical,  so  that  the  writing  lever  moves  horizontally.  For  the  purpose  of 
adjusting  the  point  of  the  writing  lever  to  any  desired  place  on  the  record- 
ing paper  the  following  movements  are  available  :  The  point  of  the  lever 
can  be  approximated  to,  or  withdrawn  from,  any  desired  point  by  means  of 
a  shding  arrangement  at  D  (Fig.  15),  where  the  stem  consists  of  two  parts 
clasping  one  another.  The  writing  point  can  be  made  to  move  in  the  hori- 
zontal direction,  so  as  to  write  at  any  desired  level  on  the  paper,  by  means 


Fig.  15.    The  tambour  with  stem  for  attachment  to  the  Dudgeon  or  Jacquet  sphygmograph. 

of  a  joint  at  E  (Fig.  15),  which  moves  stiffly,  and  retains  the  position  inVhich 
it  is  placed.  Finally,  by  rotating  the  tambour  at  a  joint  formed  where  the 
stem  is  fixed  to  the  under  surface  of  the  tambour,  the  lever  can  be  raised 
out  of  reach  during  the  adjustment  of  the  sphygmograph  to  the  pulse,  and 
brought  back  and  allowed  to  touch  the  surface  of  the  blackened  paper, 
with  sufficient  deHcacy  to  permit  its  movements  to  be  accurately  recorded 
%\ithout  being  restrained  by  too  close  pressure.  By  means  of  these  arrange- 
ments the  lever  can  be  moved  with  great  facihty  and  accuracy  in  a  vertical 
and  a  horizontal  direction,  as  well  as  made  to  approach  or  recede  from  any 
given  point.  By  this  method  any  movement  can  be  recorded  at  the  same 
time,  and  on  the  same  paper,  as  the  radial  sphygmograph.  One  can  make 
the  tambour  lever  write  directly  above  or  below  the  Avriting  lever  of  the  sphyg- 
mograph, or,  when  the  movements  are  large,  a  little  behind,  so  that  the  two 
levers  do  not  come  into  contact  during  their  excursions.  Perpendicular 
lines  to  show  the  relative  time  of  the  two  tracings  are  obtained  by  allovWng 


INSTRUMENTAL  METHODS  OF  EXAMINATION 


71 


the  lever  to  make  distinct  marks  on  the  paper  before  starting  or  after 
stopping.  With  a  pair  of  compasses,  the  relative  time  of  any  event  can  be 
accurately  gauged. 

Some  difficulty  may  be  experienced  in  the  employment  of  the  clinical 
polygraph,  on  account  of  the  weight  of  the  tambour  tilting  the  sphygmo- 
graph  off  the  radial  pulse,  especially  if  the  inelastic  band  usually  supplied 
with  the  sphygmograph  be  employed.  I  have  long  ago  abandoned  the  use 
of  the  inelastic  band  (placing  no  reliance  on  the  pressure  supposed  to  be 
required  to  obtain  an  idea  of  the  arterial  pressure),  and  employ  instead 
an  elastic  band,  tying  the  instrument  to  the  wrist  by  a  knot.  Should  any 
slipping  occur,  the  sphygmograph  and  tambour  can  readily  be  adjusted. 
It  frequently  happens  that  the  radial  pulse  causes  such  a  large  excursion 
that  there  is  no  clear  space  on  the  paper  for  the  venous  or  other  pulsation. 


Fig.  1G.  The  first  part  of  the  tracing  shows  the  venous  pulse  from  the  right  internal  jugular 
vein  (upper  tracing)  taken  at  the  same  time  as  the  radial  pulse  (lower  tracing).  The  clock- 
work being  stopped,  the  receiver  was  applied  over  the  carotid  artery,  and  tracings  of  the 
carotid  and  radial  pulses  taken.  Again  the  clockwork  was  stopped,  and  the  tambour  portion 
of  the  polygraph  removed,  and  the  full  effect  of  the  radial  pulse  was  inscribed  on  the  last 
portion. 


In  such  a  case  I  either  shift  the  sphygmograph  till  I  obtain  a  tracing  of  less 
amplitude  (seeing  that  the  object  of  taking  the  radial  pulse  at  the  same 
time  as  the  venous  is  to  obtain  an  idea  of  the  relative  time),  and,  before  the 
paper  has  entirely  passed  through,  stop  the  clockwork,  remove  the  tambour, 
and  obtain  a  fuU-sized  tracing  of  the  radial  pulse  (Fig.  16).  Or  the  venous 
pulse  may  be  taken  a  little  behind  the  radial,  and  the  various  events  dis- 
entangled. For  accurately  estimating  the  time  of  the  events,  it  is  advisable 
to  take  on  the  same  paper  a  few  beats  of  the  carotid  pulse.  For  convenience 
of  study,  other  events  can  be  readily  recorded  within  the  Umits  of  a  short 
sphygraographic  paper  ;  and  a  record  of  apex  beat,  venous,  carotid,  and 
liver  pulse  may  be  taken  at  the  same  time  as  the  radial  sphygmogram 
(Fig.  17). 

When  a  long  tracing  is  required  (as,  for  instance,  in  noting  the  move- 
ments of  the  two  sides  of  the  heart  in  cases  of  occasional  irregularity), 
a  tracing  paper  one  or  two  feet  in  length  may  be  employed. 


72 


DISEASES  OF  THE  HEART 


For  convenience,  I  have  had  the  Dudgeon  sphygmograph  altered  so  as 
to  take  a  paper  over  one  inch  in  width,  thus  allowing  more  room  for  the  two 
tracings.  At  one  time  I  had  attached  a  time-marker,  driven  by  a  separate 
clockwork  as  in  the  Jacquet,  but  this  added  too  much  to  the  weight  of  the 
machine,  so  that  it  was  easily  displaced.  Biggs  has  recently  devised  a 
convenient  Uttle  time-marker  which  can  be  fixed  to  a  Dudgeon  or  other 
sphygmograph. 

I  have  enlarged  the  box  for  holding  the  blackened  paper,  by  adding 
a  compartment  to  contain  the  tambour,  so  that  it  is  convenientl^'^  carried 
on  a  visiting  round. 


Ajiex  beat\    Carotid 


Rt.Int.J-ug. 


Fig.  17.    Apex  beat,  carotid,  right  internal  jugular,  and  liver  pulses  (upper  tracing)  taken 
at  the  same  time  as  the  radial  pulse  (lower  tracing). 

§  72.  The  ink  polygraph  (Fig.  18). — Simple  and  useful  as  is  the 
instrument  just  described,  I  found  it  was  not  convenient  when  the  move- 
ments had  to  be  recorded  over  a  long  period,  as  where  the  irregularities  were 
infrequent,  or  where  they  varied,  or  where  respiratory  curves  were  required. 
I  therefore  conceived  the  idea  of  constructing  an  instrument  that  would 
take  tracings  of  an  indefinite  length,  where  the  employment  of  ink  would 
enable  a  roll  of  paper  to  be  unwound,  and  save  as  well  the  inconvenience 
of  blackening  and  varnishing. 

I  had  considerable  difficulties  to  overcome,  but  found  a  skilled  helper 
in  Mr.  Shaw,  who  not  only  comprehended  and  appreciated  my  ideas,  but 
constructed  an  instrument  that  carried  them  out.  The  case  A  (Fig.  18) 
contains  the  clockwork  for  the  roller  which  unwinds  the  roll  of  paper  D, 
and  also  the  separate  clockwork  which  moves  the  time-marking  pen  F. 
B  B  are  the  two  tambours,  and  F  F  their  levers.  The  writing  pens  in 
Fig.  18  are  narrow-grooved  wires,  one  end  fixed  to  the  bottom  of  a  small 
cistern  at  the  free  extremity  of  the  lever.  The  other  end  of  the  grooved 
wire  is  adjusted  to  barely  touch  the  paper.  The  ink  is  put  into  the  tiny 
cistern,  and  it  flows  along  the  groove  to  the  pen  point  by  capillary  attraction. 
Recently  these  pens  have  been  greatly  improved  by  making  a  shallow 
groove  in  the  lever  act  in  place  of  the  cistern.  If  the  pens  are  kept  clean, 
and  the  ink  is  free  from  dust,  they  serve  their  purpose  most  admirably, 
and  are  ever  ready  for  use.     Red  ink  is  better  than  the  black  inks,  as  it 


INSTRUMENTAL  METHODS  OF  EXAMINATION 


73 


does  not  corrode  the  pens.  As  the  radial  pulse  is  the  most  serviceable 
of  standards,  a  special  method  is  employed  to  record  it.  A  splint  (C  1)  is 
fastened  to  the  wrist  in  such  a  manner  that  the  pad  of  the  steel  spring 
falls  on  the  radial  artery,  and  is  pressed  down  by  an  eccentric  wheel  (18) 
until  a  suitable  movement  is  transmitted  to  the  spring  by  the  artery  ; 
then  the  broad  tambour  (C)  is  fitted  on  to  the  splint  so  that  the  knob  (12) 
falls  on  the  moving  spring.  This  wrist  tambour  is  connected  to  the 
tambour  B  by  india-rubber  tubing   (22,   22),  and  the  movements  of  the 


Fig.  18.     The  ink  polygi-aph. 


radial  pulse  are  recorded  by  the  lever  F.  The  shallow  cup  (receiver)  E  is 
placed  on  the  pulsation  which  it  is  desired  to  record,  and  the  movement 
is  conveyed  to  the  lever  F  of  the  other  tambour.  In  this  way,  simul- 
taneous with  the  radial  pulse,  a  record  can  be  obtained  of  the  apex  beat, 
carotid,  jugular,  or  other  pulses. 

To  record  the  respiratory  movements,  a  bag  can  be  substituted  for  the 
receiver  E. 

By  turning  the  screw  (3)  the  rate  at  which  the  paper  passes  can  be 
quickened  or  slowed  at  will.  This  is  of  the  greatest  use,  for  it  often  happens 
that  in  quickly  succeeding  events  a  wider  interval  may  be  required,  whereas 
in  recording  respiratory  movements  a  slow  rate  is  best.    As  the  time-marker 


74  DISEASES  OF  THE  HEART 

registers  one-fiftli  of  a  second,  and  is  driven  by  a  separate  clockwork,  the 
rate  of  the  recorded  movements  can  always  be  ascertained  with  absolute 
accuracy. 

It  has  been  suggested  that  another  tambour  should  be  added  to  record 
a  third  movement,  and  I  have  tried  this  but  have  practically  discarded  it, 
as,  though  it  might  be  of  use  occasionally,  it  would  complicate  the  apparatus 
unnecessarily.  Wlien  one  is  making  observations  single-handed,  the  two 
tambours  are  quite  sufficient  to  occupy  the  attention.  With  a  little  practice 
this  apparatus  can  be  used  with  the  greatest  facility.  In  the  course  of  a  few 
minutes  the  different  movements  can  be  recorded  with  the  patient  sitting 
up  or  in  the  recumbent  position. 

When  the  tambour  is  strapped  to  the  wrist  to  take  the  radial  pulse,  one 
hand  is  always  free  to  start  the  machine,  and  to  replenish  the  ink  or  regulate 
the  rate,  the  other  hand  holding  the  receiver  over  the  movement  to  be 
recorded. 

The  tracings  in  all  the  figures  in  the  Plates  except  Figs.  90  and  103, 
and  many  in  the  text,  have  been  taken  by  this  instrument. 


CHAPTER   X 

The  Position  and  Movements  of  the  Heart 

§73.    The  jiosition  of  the  heart  in  the  chest. 

74.  The  standards  for  recognizing  the  events  in  a  cardiac  revolution. 

75.  Conditions  of  the  chest-wall  permitting  the  recognition  of  certain  movements  of   the 

heart. 

76.  The  nature  of  the  movements  graphically  recorded. 

77.  The  apex  beat. 

78.  Interpretation  of  a  tracing  of  an  apex  beat  due  to  the  systole  of  the  left  ventricle. 

79.  The  auricular  wave. 

80.  Eetraction  of  yielding  structures  in  the  neighbourhood  of  the  heart  during  ventricular 

systole. 

81.  Liver  movement  due  to  cardiac  aspiration. 

82.  Epigastric  pulsation. 

83.  The  apex  beat  due  to  the  right  ventricle. 

84.  Significance  of  the  inverted  cardiogram. 

85.  Alteration  of  the  apex  beat  due  to  retraction  of  the  lung. 

86.  The  shock  due  to  the  ventricular  systole. 

§  73.  The  position  of  the  heart  in  the  chest The  position  of  the 

heart  in  the  chest,  and  the  relations  of  its  chambers  to  the  chest-wall,  can 
best  be  reahzed  from  such  a  drawing  as  Fig.  19.  The  chief  points  to  notice 
are  the  position  of  the  apex  and  how  it  is  made'  up  of  the  left  ventricle  and 
covered  normally  by  the  lung.  The  whole  right  border  of  the  heart  is  made 
up  by  the  right  auricle,  and  the  greater  portion  of  the  anterior  surface  by 
the  right  ventricle.  The  perceptible  movements  of  the  normal  heart  when 
covered  by  the  lung  are  due  to  the  right  ventricle,  and  this  is  the  reason 
that  the  apex  beat,  due  to  the  left  ventricle,  is  not  obtained  from  people 
with  voluminous  lungs. 

§  74.  The  standards  for  recognizing  the  events  in  a  cardiac  revo- 
lution.— Owing  to  their  easy  recognition  and  determined  place  in  the  cardiac 
cycle,  the  carotid  and  radial  pulses  form  the  most  certain  standards  for 
finding  out  the  place  of  other  movements  in  a  cardiac  revolution.  In 
describing  the  tracings  frequent  references  will  have  to  be  made  to  these 
standards,  and  more  particularly  to  that  period  during  which  the  semilunar 
valves  are  open,  which  is  indicated  in  the  tracings  by  the  space  E.  When 
it  appears  in  the  radial  tracing  it  corresponds  to  the  effects  of  the  ventricular 
systole  upon  the  radial  pulse — that  is  to  say,  to  the  actual  pulse-wave — and 


76 


DISEASES  OF  THE  HEART 


not  to  the  true  time  of  the  occurrence  of  the  ventricular  systole,  for  the  pulse- 
wave  having  a  longer  distance  to  travel,  the  period  E  will  be  later  in  the 
radial  than  in  the  apex  or  carotid  tracings. 

§  75.  Conditions  of  the  chest-wall  permitting  the  recognition  of 
certain  movements  of  the  heart — The  movements  of  the  heart  in  a  healthy 
person  are  often  so  obscured  by  the  lungs,  that  only  very  little  change  is 

Arch  of  Aorta 


Sup  Vena  Cava 
Pericardium 

Aortic  Valves 
Mitral  Valves 
Right  auricle 


Tricuspid  valves 


Border  of  right 
lung 


Pulmonary  Artery 
Left  auricidar  appendage 
Pulmonary  Valves 
Pericardium 


Left  verdricle 
Right  ventricle 


Border  (f  left 
lung 


Fig.  19.     The  position  of  the  heart  in  the  chest.     (Keith.) 

discernible  in  the  external  chest-wall.  In  many  cases  the  lungs  are  so  volumi- 
nous, or  the  chest-wall  so  fat  and  thick,  that  no  movement  can  be  detected. 
But  when  a  large  surface  of  the  heart  is  directly  exposed  to  a  thin  chest-wall, 
the  heart  being  normal  or  increased  in  size,  and  the  lung  displaced,  a  series 
of  movements  of  the  chest-wall,  due  to  the  contraction  and  expansion  of 
the  heart,  can  be  recognized.  The  movements  thus  discernible  are  not  the 
same  in  all  cases,  but  depend  on  which  part  of  the  heart's  surface  comes  in 
contact  with  the  chest-wall,  and  other  yielding  structures.     These  move- 


POSITION  AND  MOVEMENTS  OF  THE  HEART  77 

ments  take  place  so  rapidly  that  it  is  difficult  to  interpret  their  significance 
by  the  unaided  senses.  Many  writers  on  this  subject  have  drawn  elaborate, 
but  nevertheless  erroneous,  conclusions  from  such  unaided  observations, 
and  it  seems  to  me  that  accurate  observations  by  the  graphic  method  alone 
can  furnish  a  clear  and  definite  explanation. 

§  76.  The  nature  of  the  movements  graphically  recorded The 

movements  of  the  heart  that  are  most  readily  recognized  are  those  connected 
with  the  systole  and  diastole  of  the  ventricles.  Movements  directly  due 
to  the  auricles  are  so  obscured  by  the  larger  and  more  vigorous  movements 
of  the  ventricle,  that  it  is  doubtful  if  they  are  ever  capable  of  recognition. 
The  movements  most  readily  recognized  are  :  first,  the  apex  beat  ;  second, 
the  filling  of  the  ventricles  ;  third,  the  emptying  of  the  ventricles  ;  and 
fourth,  the  shock  communicated  by  the  sudden  hardening  of  the  ventricular 
walls  as  they  pass  into  systole. 

§  77.  The  apex  beat — The  chief  movement,  and  the  one  which  is 
usually  most  apparent,  is  that  caused  by  the  forcible  outward  projection 
of  the  apex  of  the  heart  during  the  ventricular  systole — the  apex  beat. 
This  is  generally  described  as  '  the  lowest  and  outermost  point  of  the  heart 
which  strikes  against  the  chest-wall '.  In  healthy  adults,  it  is  usually  felt 
in  the  fifth  left  intercostal  space,  immediately  inside  the  nipple  line.  It 
may,  however,  be  situated  in  the  fourth  interspace,  and  outside  the  nipple 
line  in  children,  and  in  some  adults.  In  disease  of  the  heart  it  alters  its 
situation  with  the  increasing  size  of  the  heart.  This  forward  thrust  occurs 
when  the  left  ventricle  is  in  contact  with  the  chest.  As  will  be  shown  later, 
a  movement  of  another  description  occurs  when  the  right  ventricle  consti- 
tutes the  so-called  apex  beat.  That  the  apex  beat  due  to  the  left  ventricle 
is  a  distinct  displacement  of  the  heart  forward  can  be  recognized  by  the 
senses  of  touch  and  sight. 

During  the  whole  time  occupied  by  the  systole  of  the  ventricle,  the  apex 
is  usually  kept  projecting  into  the  interspace,  so  that  the  palpating  hand 
recognizes  the  forward  thrust,  and  in  such  a  tracing  as  Fig.  20,  the  lever 
taking  the  tracing  is  kept  raised  during  the  whole  time  of  the  outflow 
from  the  ventricle  (space  E').  If  the  left  ventricle  is  much  hypertrophied, 
the  same  movement  can  sometimes  be  detected  in  two  or  three  interspaces. 
If  the  interspaces  be  fairly  open  and  the  chest-wall  thin,  and  the  tip  of  the 
finger  be  thrust  into  the  third  or  fourth  interspace  near  the  sternum,  the 
right  ventricle  can  be  felt  hardening,  and  remaining  thus  hardened  in  contact 
with  the  finger  during  the  whole  period  of  the  ventricular  systole.  It  cannot, 
however,  be  averred  that  in  this  case  there  is  a  forward  thrust.  The  heart 
here  is  always  in  contact  with  the  chest-wall,  and  the  finger  pushed  into  the 


78  DISEASES  OF  THE  HEART 

interspace  during  the  diastole  in  all  likelihood  impinges  against  the  lax 
ventricular  wall.  As  soon  as  the  ventricle  hardens,  the  finger  recognizes 
this  hardening  as  something  pushing  against  it.  This  sensation  of  a  thrust 
is  sometimes  actually  s3niclironous  with  an  indrawing  of  the  soft  structures 
filling  up  the  interspace  (Fig.  26). 


Fig.  20.  Simultaneous  tracings  of  the  apex  beat  and  the  carotid 
pulse,  showing  the  '  systolic  plateau  '  in  the  cardiogram  during  the 
outflow  from  the  ventricle  {E'). 

§  78.  Interpretation  of  a  tracing  of  an  apex  beat  due  to  the  systole 
of  the  left  ventricle. — A  tracing  of  the  apex  beat  or  cardiogram  is  a  diagram- 
matic representation  of  (a)  the  forward  movement  of  the  apex  of  the  heart 
while  the  ventricular  muscle  is  beginning  to  contract  (space  D,  Fig.  21)  ; 


Fig.  21.  Simultaneous  tracings  of  the  apex  beat  and  of  the  pulsation  in  the  pulmonary 
artery,  a  represents  the  small  wave  due  to  the  auricular  systole.  The  time  during  which  the 
ventricle  is  passing  into  systole  is  represented  by  the  space  (D),  emptying  (E),  relaxing  (F), 
filling  (G).  While  this  tracing  was  being  taken  the  cylinder  was  rapidly  rotated.  The  letters 
D,  E,  F  have  reference  to  the  same  periods  in  the  cardiac  revolution  as  in  Fig.  43  (see  p.  108). 

(6)  the  retention  of  the  apex  beat  against  the  chest-wall  while  the  ventricles 
are  emptying  (space  E,  Fig.  21)  ;  (c)  the  backward  movement  of  the  apex 
of  the  heart  while  the  ventricular  muscle  is  relaxing  (space  F,  Fig.  21)  ; 
{d)  and  the  gradual  swelling  of  the  ventricle  during  diastole  (space  G,  Fig.  21). 
(a)  The  period  of  commencing  contraction  of  the  ventricular  muscle — the 
presphygmic  interval  (space  D,  Fig.   21). — During  this  period  the  pressure 


POSITION  AND  MOVEMENTS  OF  THE  HEART 


79 


within  the  ventricle  is  rapidly  rising.  The  auriculo-ventricular  valves  close 
as  soon  as  the  pressure  within  the  ventricle  rises  above  that  in  the  auricle, 
and  the  semilunar  valves  open  as  soon  as  the  pressure  in  the  ventricle 
rises  above  that  in  the  aorta.  This  last  occurs  at  the  end  of  the  period  D, 
Fig.  21,  and  is  usually  indicated  by  the  abrupt  termination  of  the  upstroke. 
In  Fig.  21  simultaneous  tracings  were  taken  of  the  pulsation  in  the  pul- 
monary artery  and  of  the  apex  beat.     As  the  beginning  of  the  pulse  in  the 


Fig.  22.  Simultaneous  tracings  of  the  apex  beat  and  of 
the  pulsation  in  the  pulmonary  artery.  The  letters  have  the 
same  significance  as  those  in  Fig.  21. 

pulmonary  artery  indicates  the  opening  of  the  semilunar  valves,  so  it  is 
found  that  the  end  of  the  period  D  corresponds  exactly  with  the  beginning 
of  the  pulsation  of  the  pulmonary  artery.  When  this  figure  was  taken  the 
cylinder  was  rotated  rapidly  in  order  to  separate  the  events  as  widely  as 
possible.  When  the  cyHnder  rotates  at  a  slower  rate,  this  period  is  repre- 
sented by  an  almost  perpendicular  line  (Fig.  22). 


Fig.  23.    Simultaneous  tracings  of  the  pulses  of  the  carotid  and  pulmonary  arteries. 
After  the  third  beat  the  cylinder  was  rotated  rapidly. 

It  will  be  noted  that  the  termination  of  the  upstroke  corresponds  exactly 
with  the  beginning  of  the  outjBlow  of  the  ventricle  into  the  artery.  These 
tracings  were  taken  from  a  lad  suffering  from  phthisis  of  the  left  lung,  which 
had  retracted  from  the  heart,  and  through  the  thin  chest -walls  the  various 
movements  could  easily  be  observed.  In  the  second  left  interspace  there 
was  a  marked  pulsation,  and  tracings  of  this,  taken  at  the  same  time  as  the 
carotid  pulse,  left  no  doubt  as  to  its  being  caused  by  the  pulmonary  artery 
(Fig.  23).     It  will  be  noticed  that  the  carotid  pulse  appears  just  a  very  little 


80  DISEASES  OF  THE  HEART 

later  than  the  pulmonary.  Here  also,  after  a  few  beats,  the  cylinder  was 
rapidly  rotated  with  the  hand  to  separate  more  widely  the  different  events. 

(6)  The  period  of  ventricular  outfloio  (space  E,  Fig.  21). — When  the 
pressure  in  the  ventricles  exceeds  that  in  the  aorta  and  pulmonary  artery 
the  semilunar  valves  open,  and  the  blood  flows  out  from  the  ventricles. 
During  this  period  the  apex  is  usually  kept  stationary,  pressing  against  the 
chest-wall,  and  in  many  tracings  (as  in  Fig.  24)  it  is  shown  by  a  fairly  level 
line — the  systolic  '  plateau  '.  In  place  of  a  flattened  top  representing  the 
period  of  ventricular  outflow,  the  tracing  may  continue  to  rise  (as  in  Fig.  20), 
indicating  that  the  ventricle  is  still  slightly  shifting.  On  the  other  hand, 
the  tracing  sometimes  rapidly  descends  (Figs.  21  and  22).  I  cannot  but 
think  that  this  is  due  to  the  ventricle  shrinking  away  from  the  interspace 
during  its  systole,  the  receiver  perhaps  not  being  exactly  over  the  apex. 
I  shall  show  later  on  that  this  shrinking  can  be  demonstrated  in  various 
places,  and  I  have  found  evidence  of  it  immediately  under  a  diffuse  apex 
beat.  The  movement  producing  the  apex  beat  is  really  a  displacement 
of  the  heart  forward,  and  while  the  heart  is  thus  displaced  the  ventricles 
shrink  as  they  empty  themselves  (see  §  20).  The  termination  of  the  ven- 
tricular outflow  is  occasioned  by  the  pressure  in  the  aorta  becoming  higher 
than  that  in  the  ventricle.  The  semilunar  valves  close  in  consequence, 
and  the  ventricular  muscle  then  relaxes  ;  the  termination  of  the  systolic 
period  is  indicated  in  the  cardiogram  by  a  sudden  descent. 

(c)  The  period  of  relaxation  of  the  ventricular  muscle  (space  F,  Fig.  21). 
— With  the  relaxation  of  the  ventricular  muscle  the  apex  retreats  from 
the  chest-wall,  as  is  indicated  by  the  slanting  downstroke  in  the  tracing, 
or  where  the  tracing  is  already  falling  during  the  ventricular  outflow  by 
a  more  rapid  descent  (Figs.  21  and  22).  During  this  period  the  ventricular 
pressure  rapidly  falls  until  the  stage  of  complete  relaxation,  when  the 
pressure  inside  the  ventricles  becomes  lower  than  that  inside  the  auricles. 
Wlien  this  occurs  the  auriculo-ventricular  valves  open.  The  apex  then 
has  reached  its  greatest  distance  from  the  chest-wall,  and  in  the  tracing  the 
lowest  point  is  reached. 

The  time  of  the  opening  of  the  auriculo-ventricular  valves  is  usually 
a  very  definite  landmark  in  apex  and  jugular  tracings,  and,  in  consequence, 
is  a  useful  standard  for  measuring  the  sequence  of  events  in  tracings  of 
irregular  heart  action.  It  is  recognized  as  the  lowest  point  reached  in  tracings 
of  the  apex  of  the  left  ventricle,  and  it  is  just  before  the  fall  of  the  wave  v, 
in  tracings  of  the  jugular  pulse.  Its  time  corresponds  nearly  with  the  bottom 
of  the  aortic  notch  in  tracings  of  the  radial  pulse.  It  is  represented  by  the 
perpendicular  line  6  in  man^^  of  the  tracings  given  later. 


POSITIOX  AXD  MOVEMENTS  OF  THE  HEART  81 

(d)  The  period  of  filling  of  the  ventricles  (space  G,  Fig.  21). — Upon 
the  opening  of  the  auriculo-ventricular  valves,  the  blood  flows  from  the 
auricles  into  the  ventricles,  and  as  the  ventricles  distend  the  heart  pushes 
against  the  intercostal  space,  and  slightly  raises  the  lever.  Tliis  period  is 
marked  in  the  tracing  by  a  gradual  ascent.  Frequently,  however,  the  heart 
fails  to  affect  the  tissues  in  the  interspace  during  this  period,  so  that  no 
indication  of  the  filhng  of  the  ventricles  is  obtained  ;  in  such  a  tracing  as 
Fig.  20,  for  example,  and  in  many  others  given  in  the  text,  the  whole  of  this 
■period  is  a  blank,  so  far  as  information  regarding  events  in  the  cardiac 
cycle  are  concerned. 

§  79'  The  auricular  wave — In  some  tracings  from  the  apex  there 
is  occasionally  found  an  abrupt  though  slight  rise  immediately  preceding 
the  beginning  of  the  ventricular  systole  {a,  Figs.  21  and  24).     This  is  due  to 


Fig.  24.  Simultaneous  tracings  of  the  apex  beat  and  of  the 
radial  pulse,  showing  the  '  systolic  plateau  '  and  the  small  wave 
(a)  due  to  the  auricular  systole.  The  third  beat  in  the  apex  tracing 
is  obliterated  by  the  movement  of  inspiration. 

a  sudden  increase  in  the  contents  of  the  ventricle  caused  by  the  contraction 
of  the  auricle,  and  may  be  termed  the  auricular  wave. 

The  auricular  wave  is  not  always  perceptible  in  apex  tracings,  but  when 
present  it  often  gives  valuable  information.  Normally,  it  precedes  the  begin- 
ning of  the  wave  due  to  the  ventricular  systole  by  about  one-tenth  of  a  second 
(space  between  1  and  2,  Fig.  25).  Sometimes  this  interval  is  increased, 
and  then  it  may  indicate  a  delay  in  the  passage  of  the  stimulus  from  auricle 
to  ventricle  (Fig.  231,  p.  339).  In  cases  of  heart-block,  it  may  be  recognized 
during  the  ventricular  pauses  (Fig.  123).  Its  absence  may  be  of  no  signi- 
cance,  but  it  is  to  be  noted  that  it  is  never  seen  in  cases  with  the  nodal 
rhythm,  even  when  immediately  before  the  starting  of  this  abnormal  rhythm 
it  had  been  a  conspicuous  feature  (compare  Fig.  198  with  Fig.  202,  p.  332). 

§  8o.  Retraction  of  yielding  structures  in  the  neighbourhood  of 
the  heart  during  ventricular  systole — When  the  ventricles  expel  their 
contents  they  must  of  necessity  shrink.  This  shrinkage  occurs  abruptly, 
and  with  considerable  force.  The  yielding  tissues  in  the  neighbourhood 
of  the  heart  are  dragged  upon,  and  evidence  of  this  dragging  can  be  obtained 

MACKENZIE  n 


82 


DISEASES  OF  THE  HEART 


from  a  variety  of  sources.  John  Hunter  ^^^  originated  the  idea  that  the 
systole  of  the  ventricles  would  have  a  tendency  to  produce  a  vacuum,  and 
thus  expedite  the  flow  of  the  venous  blood  into  the  chest.  Evidence  of 
this  '  cardiac  aspiration  '  affecting  the  lungs  has  been  obtained  by  a  number 
of  observers.     The  tracings  ^'^^  of  Mosso  and  Delepine  ^^^  of  the  movements  of 


Fig.  25.  The  apex  tracing  shows  a  slight  wave,  a,  due  to  the  contraction  of  the  auricles 
distending  the  ventricles  and  beginning  one-tenth  of  a  second  before  the  ventricular  systole. 
For  explanation  of  the  numbered  perpendicular  lines  see  Fig.  46. 

the  column  of  air  in  the  respiratory  passages,  due  to  the  cardiac  aspiration, 
correspond  exactly  with  those  obtained  from  the  praecordium  (Eig.  26), 
from  under  the  liver  (Figs.  27  and  28),  and  from  the  epigastrium  (Figs. 
29  and  30). 


Fig.  26.  Simultaneous  tracings  of  the  heart  movements  (upper  tracing) 
and  of  the  radial  pulse.  The  first  part  of  the  upper  tracing  was  taken  from  the 
apex  beat  in  the  fourth  interspace  immediately  outside  the  nipple,  while  the 
latter  part  was  taken  in  the  same  interspace  near  the  left  border  of  the  sternum. 
In  the  first  part  the  cardiogram  shows  a  '  systolic  plateau  '  during  the  ventricular 
outflow  {E),  in  the  other  part  the  cardiogram  is  inverted,  i.  e.  there  is  a  depres- 
sion during  this  period  {E). 

In  Fig.  26  this  drawing-in  of  tissues  in  the  intercostal  spaces  over  the 
heart  is  demonstrated.  It  was  obtained  from  a  boy  aged  fourteen.  The 
apex  beat  was  well  marked  in  the  fourth  interspace  outside  the  nipple.  At 
the  same  time  that  the  apex  was  thrust  outwards,  the  skin  and  subcutaneous 
tissues  over  the  same  interspace  inside  the  nipple  were  drawn  in.  In  Fig.  26 
the  tracings  of  the  apex  beat  were  taken  simultaneously  with  the  radial 


POSITION  AND  MOVEMENTS  OF  THE  HEART  83 

pulse  for  four  beats.  The  clockwork  was  then  stopped,  and  the  receiver, 
which  had  been  applied  over  the  apex,  was  placed  over  the  praecordium 
inside  the  nipple,  and  the  '  inverted  cardiogram  '  of  the  last  portion  was 
obtained.  The  space  E  represents  the  duration  of  the  outflow  from  the 
ventricle  ;  and  this  period,  which  in  the  apex  tracing  shows  a  flattened 
elevation,  shows  a  great  depression  in  that  obtained  from  the  front  of  the 
heart.  The  ascending  limb  of  the  apex  tracing  corresponds  to  the  period 
during  which  the  ventricle  is  contracting  (space  D,  Fig.  21).  This  period 
in  the  inverted  cardiogram  is  represented  by  a  slight  rise,  due  to  the  shock 
of  the  contracting  ventricle.  No  blood  as  yet  has  escaped  from  the  ventricle. 
As  soon  as  the  semilunar  valves  open  the  blood  rushes  out  of  the  ventricle, 
the  ventricles  diminish  in  size  and  the  yielding  tissues  of  the  interspace 
sink  in  and  cause  the  great  fall,  as  represented  in  the  inverted  cardiogram 
(space  E,  in  the  latter  half  of  Fig.  26). 

§  8i.  Liver  movements  due  to  cardiac  aspiration Not  only  can 

this  aspiration  be  demonstrated  as  affecting  the  pliable  tissues  immediately 
in  contact  with  the  heart,  but  in  suitable  cases  it  can  be  shown  to  produce 
a  distinct  excursion  of  the  liver.  All  writers  referring  to  this  movement 
of  the  liver  speak  of  it  as  a  downward  thrust  during  the  ventricular  systole. 
Careful  tracings  demonstrate  that  this  movement  is  quite  of  the  opposite 
nature — it  is  a  dra wing-up  of  the  liver  during  the  ventricular  systole.  In 
Figs.  27  the  apex  beat  is  taken  at  the  same  time  as  the  movement  of  the 
liver. 

The  receiver  taking  the  liver  movement  being  applied  to  the  under  surface 
of  the  organ,  a  retraction  of  the  liver  upwards  corresponds  with  a  fall  in 
the  tracing,  and  vice  versa.  It  will  be  seen  that  the  movement  m  the  liver 
upwards  takes  place  during  the  ventricular  systole,  while  the  downward 
movement  is  due  to  the  diastolic  filling  of  the  ventricle.  In  Fig.  28  the 
movement  of  the  liver  is  recorded  at  the  same  time  as  the  carotid  pulse. 
It  is  seen  that  as  soon  as  the  carotid  pulse  appears,  the  liver  is  drawn  up, 
and  remains  there  until  the  end  of  the  ventricular  systole,  after  which 
the  liver  gradually  faUs  down.  I  do  not  mean  that  the  excursion  of  the  liver 
is  one  of  considerable  extent,  but  the  movement  is  so  great  as  to  be  obvious 
to  the  palpating  hand.  It  is  distinct  from  a  pulsation  of  the  Uver,  which 
is  a  periodic  swelling  of  the  liver,  while  this  is  a  displacement  of  the  hver 
en  masse. 

§  82.    Epigastric  pulsation — The  causes  which  may  produce  a  pulsation 

in  the  epigastrium  are  :    (a)  a  dilated  right  heart  ;    (6)  a  hypertrophied  left 

ventricle  ;    (c)  the  abdominal  aorta  ;   and  [d)  an  aneurysm  of  the  abdominal 

aorta. 

g2 


84 


DISEASES  OF  THE  HEART 


In  the  later  stages  of  typhoid  fever  and  other  exhausting  diseases, 
epigastric  pulsation  is  an  ominous  sign  of  cardiac  enfeeblement.  The 
movement  consists  of  an  alternate  swelling  and  retraction  of  the  epigastrium. 
It  is  invariably  assumed  that  this  swelling  or  pulsation  is  due  to  the  right 


Fig.  27.  Simultaneous  tracings 
of  the  apex  beat  and  of  the  move- 
ment of  the  liver.  When  the 
ventricle  empties  the  liver  is  drawn 
up,  and  this  causes  the  fall  in  the 
tracing. 


'  Fig.  28.  Simultaneous  tracings  of  the 
carotid  pulse  and  liver  movement.  With 
the  ajipearance  of  the  carotid  pulse  there 
is  a  sudden  fall  of  the  lower  tracing  due  to 
the  liver  being  drawn  upwards  by  the 
emptying  ventricles. 


ventricular  systole,  and  that  it  is  of  the  same  nature  as  the  outward  protrusion 
constituting  the  apex  beat.  If  this  form  of  epigastric  pulsation  is  carefully 
timed  wi|[i  the  carotid  pulse,  it  will  be  found  that  the  epigastric  pulse,  pro- 
trusion, or  swelling,  precedes  the  carotid  pulse,  and  that  the  retraction  of 


iWj 

e\           Spiga^stric  Pulsa-tion 
Ra.dia,l 

^        CaLTottd 

Fig.  ^29.  Simultaneous  tracing  of  the  epigastric  pulse,  due  to  a  dilated  right  heart, 
and  of  the  radial  pulse.  The  epigastric  pulse  shows  a  retraction  during  the  ventricular 
systole  {E),  and  a  jDrotrusion  during  the  filling  of  the  ventricle. 


the  epigastrium  corresponds  in  time  to  the  carotid  pulsation.  The  apex 
beat  is  rarely  available  in  these  cases,  on  account  of  the  right  heart  pushing 
the  left  ventricle  backwards.  In  the  tracings  of  the  epigastric  pulse  (Fig. 
29)  the  radial  pulse  is  taken  as  the  standard  of  time.     The  time  occupied 


POSITION  AND  MOVEMENTS  OF  THE  HEART 


85 


by  the  pulse  travelling  from  the  heart  to  the  wrist  being  allowed  for,  it  will 
be  found  that  the  great  fall  in  the  epigastric  pulse  corresponds  exactly  with 
the  ventricular  systole  (E). 

The  patient  from  whom  this  tracing  was  taken  was  dying  from  pernicious 
anaemia.  At  the  post-mortem  examination,  a  needle  pushed  through  the 
epigastrium,  at  the  place  where  the  tracing  was  obtained,  was  found  to  have 
penetrated  the  right  ventricle. 


ric  PulscLtion  


Fig.  30.  Shows  the  same  features  as  Fig.  29,  with  the  excej)lion  of 
the  small  wave  (c)  occasioned  by  the  shock  communicated  to  the  epigas- 
trium by  the  abdominal  aortic  pulse.  A  few  beats  of  the  abdominal  aorta 
are  also  given. 

In  Fig.  30  a  similar  tracing  is  given,  except  that  there  is  a  slight  inter- 
ruption at  c,  on  the  line  of  descent.  This  will  be  found  to  correspond  exactly 
to  the  time  of  the  abdominal  aorta,  taken  from  the  middle  of  the  abdomen, 
a  few  beats  of  which  are  also  given.  This  small  wave  (c)  is  due  to  the  impulse 
imparted  to  the  tissues  by  the  pulse  of  the  underlying  aorta.  Epigastric 
pulsation,  due  to  hyper trophied  left  ventricle,  has  the  same  character  as  an 
apex  beat  (Fig.   31).      Epigastric  pulsation  due]  to  the  abdominal  aorta 


ApeocBeat 


Epigastric  Puls&tion 


Fig.   31.     Simultaneous  tracings   of  the   apex   beat   and  of  the 
epigastric  pulsation,  due  to  a  hypertrophied  left  ventricle. 

]3resents  quite  a  different  character  from  that  due  to  a  dilated  right  ventricle, 
as  shown  in  Fig.  32,  where  the  pulse  corresponds  in  character  and  time 
with  the  radial  pulse.  An  epigastric  pulsation  due  to  an  aneurysm  of  the 
abdominal  aorta  would  assume  the  time  and  character  of  the  abdominal 
aortic  pulse  (Fig.  32). 

§  83.  The  apex  beat  due  to  the  right  ventricle — Accepting  the  usual 
clinical  definition  of  the  apex  beat  '  being  the  lowest  and  outermost  part  of 
the  heart's  impulse  ',  a  totally  different  form  of  beat  is  found  when  the  right 


86 


DISEASES  OF  THE  HEART 


ventricle  causes  this  movement.  In  certain  cases  of  dilatation  of  the  right 
heart,  nearly  the  whole  anterior  aspect  of  the  heart  is  composed  of  the  right 
auricle  and  ventricle,  the  left  ventricle  forming  but  a  mere  strip  of  the  border 
(see  Figs.  135  and  136).  This  portion  of  the  left  ventricle  is  situated  so  far 
back  that  it  is  covered  by  the  lungs,  and  does  not  reach  the  chest-wall. 
Hence  it  is  that  '  the  lowest  and  outermost  part  of  the  heart '  in  contact 


Epig-PuLlsatioTx 

/ 

HwJ---^-i^-~i^ 

lj^^=::i^ 

Radial 

Fig.  32.    Simultaneous  tracings  of  the  epigastric  pulse,  due  to 
the  abdominal  aorta,  and  of  the  radial  pulse. 

with  the  chest-wall  is  the  right  ventricle.  The  character  of  the  apex  beat 
now  corresponds  exactly  with  that  of  the  Uver  movements,  of  the  epigastric 
pulse,  due  to  enlarged  right  heart,  and  of  the  inverted  cardiogram  in  Fig.  26. 
In  place  of  the  outward  thrust  during  the  systole,  as  in  the  apex  beat  due  to 
the  left  ventricle,  there  is  an  indrawing  of  the  tissues. 


Fig.  33.  Tracings  of  the  apex  beat,  jugular  pulse,  and  carotid  pulse  (upper  tracing),  taken 
at  the  same  time  as  the  radial.  The  apex  tracing  is  due  to  the  right  ventricle,  and  shows 
a  depression  {E)  during  the  ventricular  outflow.  The  sharp  elevation  preceding  E  is  caused 
by  the  shock  of  the  contracting  ventricles.  This  is  preceded  by  a  small  wave  (o),  which  is  due 
to  the  contracting  auricle  distending  the  ventricle,  and  corresponds  in  time  exactly  with  the 
wave  (a)  in  the  jugular  pulse,  which  is  due  to  the  contracting  auricle  sending  a  wave  of  blood 
back  into  the  veins. 

Fig.  33  was  taken  from  a  youth,  aged  eighteen,  with  simple  dilatation 
of  the  heart,  and  free  from  valvular  disease.  There  was  marked  pulsation 
of  the  jugular  veins,  a  few  beats  of  which  are  given.  The  apex  tracing  shows 
a  great  depression  during  the  period  of  ventricular  outflow  {E).  This  period 
is  immediately  preceded  by  an  abrupt  rise  due  to  the  shock  communicated 
to  the  chest  by  the  sudden  hardening  of  the  ventricular  wall.  Although 
corresponding  with  the  period  D  (Figs.  21  and  22)  in  the  left  ventricular 
apex  tracings,  I  am  inclined  to  think  that  the  rise  here  is  an  instrumental 


POSITION  AND  MOVEMENTS  OF  THE  HEART  87 

fault,  due  to  the  violent  shock  communicated  by  the  sudden  and  forcible 
ventricular  contraction.  This  period  is  preceded  by  a  small  wave  (a)  in  the 
tracing  identical  with  the  similar  rise  in  Figs.  24  and  25  of  the  left  ventricular 
apex  beat.  It  is  due  in  this  case,  as  in  those,  to  the  distension  of  the  ventricle 
by  the  auricular  systole.  It  occupies  exactly  the  same  period  in  the  cardiac 
revolution  as  the  wave  (a)  in  the  venous  pulse,  which  is  produced  by  the 
systole  of  the  right  auricle.  The  space  E  in  all  the  tracings  represents  the 
period  of  ventricular  outflow  as  it  affects  the  different  pulses.  One  can, 
therefore,  readily  and  with  certainty  refer  the  different  events  to  their  causes. 
Thus  we  know  that  the  wave  of  contraction  arising  in  the  auricle  passes  on  to 
the  ventricle,  that  between  the  auricular  outflow  and  the  ventricular  outflow 
a  period,  the  presphygmic  {D,  Fig.  21),  exists,  during  which  the  ventricle 
is  contracting  and  raising  its  pressure  until  it  opens  the  semilunar  valves. 
Thus  the  presphygmic  period  in  the  apex  tracing  exactly  corresponds  to  the 
period  between  the  summit  of  the  wave  a  in  the  venous  pulse  due  to  the 
auricular  systole,  and  that  of  the  wave  c  due  to  the  carotid  pulse.  A  few 
beats  of  the  carotid  are  given,  which  can  be  taken  as  a  standard  of  time  to 
verify  all  these  points.     The  period  G  is  due  to  the  filling  of  the  ventricle. 

§  84.  Significance  of  the  inverted  cardiogram It  is  asserted  in 

textbooks  that  an  indrawing  of  the  apex  during  systole  of  the  ventricles  is 
a  diagnostic  sign  of  adherent  pericardium.  I  have  had  several  cases  where 
I  have  got  at  one  time  tracings  of  the  apex  beat  due  to  the  left  ventricle, 
and  at  other  times  tracings  due  to  the  right  ventricle,  with  indrawing  during 
systole  ;  and  at  the  post-mortem  examination  there  has  never  been  found 
any  signs  of  adherent  pericardium. 

The  fact  that  '  the  lowest  and  outermost  point  of  the  heart  which  strikes 
against  the  chest-wall '  may  be  due  to  the  right  ventricle  should  be  borne 
in  mind.  Whenever  that  occurs,  the  cardiogram  is  an  inverted  one — that 
is  to  say,  there  is  a  shrinking  of  the  heart  from  the  chest-wall  during  the 
systole  and  a  protrusion  during  the  diastole  of  the  ventricles.  This  is  not 
always  recognizable  at  first  sight.  Being  somewhat  familiar  with  the 
form  of  various  apex-beat  curves,  I  generally  have  no  difficulty  in  recog- 
nizing cardiograms  due  to  the  left  ventricle.  But  when  from  a  patient 
I  took  Fig.  34,  I  certainly  was  misled  in  the  first  instance.  The  abrupt  rise 
and  fall  bear  a  close  resemblance  to  an  apex-beat  curve  due  to  the  left  ven- 
tricle. Careful  measurements  of  the  radial  and  apex  tracings  show  that  the 
elevation  in  Fig.  34  was  not  at  the  period  of  ventricular  systole,  but  occurred 
during  ventricular  diastole,  while  the  systolic  period  {E)  corresponded  with 
the  fall  in  the  tracing.  It  is  necessary  to  insist  upon  this  view,  because 
inferences  drawn  from  the  apex  beat  alone  are  liable  to  lead  one  into  error. 


88  DISEASES  OF  THE  HEART 

Even  so  careful  an  observer  as  Keyt  ^^'^  has  mistaken  the  nature  of  such  an 
apex-beat  tracing,  and.  imagined  in  consequence  that  he  detected  an  extreme 
delay  in  the  appearance  of  the  arterial  pulse.  I  have  observed  similar 
errors  of  interpretation  in  the  tracings  of  other  %^Titers.  It  follows  then 
that  for  a  guide  to  any  event  occurring  during  a  cardiac  revolution  the 
arterial  pulse  is  the  only  safe  and  reliable  one.  When  the  apex  beat  is 
taken  as  a  standard,  careful  inquiries  should  be  directed  to  ascertain  its 
true  nature.  While  it  is  true  in  the  majority  of  instances  that  the  cardio- 
gram from  the  right  ventricle  is  '  inverted  ',  I  have  taken  tracings  with 
a  systolic  plateau  from  the  third  and  fourth  interspaces  near  the  sternum, 
but  as  I  have  had  no  post-mortem  examination  in  these  cases  I  am  not  sure 
of  the  part  of  the  heart  producing  these  curves.  The  whole  subject  of 
cardiography  is  in  great  need  of  thorough  and  painstaking  investigation. 


Apex  beat\ 


Radial 


^-J^^ 


Fig.  34.  Simultaneous  tracings  of  the  apex  beat  and  of  the  radial 
pulse.  The  rise  in  the  apex  tracing  resembles  the  usual  characters 
present  in  a  tracmg  of  the  apex  beat  due  to  the  left  ventricle.  On 
analysis  it  is  found  that  the  elevation  is  during  the  diastole,  and  the 
fall  (E)  during  the  systole,  of  the  ventricle. 

§  85.  Alteration  of  the  apex  beat  due  to  retraction  of  the  lung. — 

If  one  watches  the  progress  of  a  case  of  advancing  heart  failure  over  a  period 
of  years,  marked  changes  -sviU  sometimes  be  detected  not  only  in  the  character 
but  in  the  position  of  the  apex  beat.  In  the  earlier  stages  of  heart  failure, 
due  to  mitral  disease,  for  instance,  the  left  ventricle  may  be  pushed  back 
by  the  distended  right  ventricle,  so  that  it  is  entirely  covered  by  the  lung, 
and  the  apex  beat  may  then  be  due  to  the  right  ventricle.  In  course  of  time, 
from  pressure  of  the  enlarged  heart,  the  lung  is  compressed  and  recedes, 
leaving  a  large  surface  of  the  heart  bare  to  the  chest -wall.  In  such  cases 
the  apex  beat  may  be  found  in  the  posterior  axillary  line  and  in  the  eighth 
interspace.     The  tracing  obtained  then  is  one  due  to  the  left  ventricle. 

§  86.  The  shock  due  to  the  ventricular  systole I  am  of  opinion 

that  a  good  deal  of  confusion  in  regard  to  the  correct  interpretation  of  the 
heart  movements  has  arisen  from  associating  the  shock  conveyed  to  the 
chest-wall,  when  the  ventricles  pass  into  systole,  with  the  apex  beat.  The 
apex  beat  and  this  impulse  have  become  so  connected  that  it  is  assumed 


POSITION  AND  MOVEMENTS  OF  THE  HEART  89 

that  they  are  one  and  the  same  thing.  The  apex  beat  due  to  the  left  ven- 
tricle is  a  movement  which  lasts  during  the  whole  of  the  ventricular  systole  ; 
the  shock  caused  by  the  ventricular  contraction  endures  but  a  short  space 
of  time,  and  occurs  while  the  ventricular  muscle  suddenly  hardens  and 
corresponds  with  the  upstroke  only  of  the  apex  beat  {D,  Figs.  21  and  22). 
It  is  this  shock  which  sends  the  lever  so  high  in  Figs.  24  and  33,  at  the 
beginning  of  the  ventricular  contraction.  In  the  tracings  of  the  epigastric 
pulse  (Figs.  29  and  30),  and  of  the  movement  from  the  front  of  the  heart 
(Fig.  26),  this  shock  causes  the  sharp  elevation  just  before  the  faU  [E)  due  to 
the  emptying  of  the  ventricle.  Thus,  in  noting  the  time  of  the  shock  and 
watching  the  epigastric  pulse,  for  instance,  as  in  Figs.  29  and  30,  one  could 
see  that  the  retraction  of  the  epigastrium  followed  it.  If  one  associated 
the  shock  with  the  apex  beat,  it  would  therefore  be  assumed  that  the  pro- 
trusion corresponded  with  the  systole,  and  the  retraction  with  the  diastole. 
It  frequently  happens  that  this  shock  is  the  only  movement  of  the  heart 
discernible  on  examining  the  chest.  It  is  often  markedly  present  in  dilata- 
tion of  the  heart,  when  the  heart's  surface  in  contact  with  the  chest-wall  is 
entirely  made  up  of  the  right  ventricle  and  auricle.  In  such  cases  it  must 
not  be  assumed  that  the  shock  is  the  evidence  of  the  contraction  of  the 
right  ventricle  only.  It  is  impossible  to  distinguish  the  shock  due  to  the 
right  ventricle  from  the  shock  due  to  the  left.  The  reason  I  insist  upon 
this  is  because  the  perception  of  this  shock  has  been  assumed  to  be  an  evidence 
of  the  right  heart  contracting  when  the  absence  of  a  beat  in  the  radial  pulse 
was  supposed  to  indicate  the  absence  of  a  contraction  in  the  left  ventricle. 
As  will  be  shown  later,  this  sort  of  evidence  is  not  only  unreliable  but 
actually  misleading. 


CHAPTER  XI 

Examination  of  the  Arterial  Pulse 

§  87.  Superiority  of  the  digital  examination. 

88.  What  is  the  pulse  ? 

89.  Inspection  of  the  arteries. 

90.  Digital  examination  of  the  arteries. 

91.  The  value  of  a  sphygmogram. 

92.  Definition  of  a  sphygmogram. 

93.  Events  occurring  during  a  cardiac  revolution  revealed  by  the  sphygmogram 

(a)  the  systolic  period,  (b)  the  diastolic  period. 

94.  Features  of  the  sphygmogram  due  to  instrumental  defect. 

§  87.  Superiority  of  the  digital  examination In  the  examination 

of  the  arterial  pulse,  several  methods  may  be  employed,  as  exploration  by 
the  finger,  by  graphic  records,  and  by  instrumental  measurement  of  the 
arterial  pressure.  By  far  the  most  important  of  these  methods  is  the  first. 
There  is  a  tendency  to  exalt  the  others  at  the  expense  of  the  digital,  but  no 
apparatus  can  ever  replace  the  trained  finger.  No  doubt  the  other  methods 
can  give  very  definite  information  of  a  limited  kind,  but  in  diagnosing  the 
patient's  condition,  they  should  only  supplement  the  digital  examination. 

The  mechanical  methods  can  be  of  use,  however,  in  enabling  us  to 
appreciate  the  meaning  of  the  sensation  felt  by  the  finger,  and  the  attempt 
should  always  be  made  to  correlate  these  sensations  with  the  results  obtained 
by  the  more  elaborate  means. 

Warning  must  be  given  against  estimating  the  patient's  condition  by 
the  study  of  the  pulse  alone  ;  any  definite  result  obtained  must  only  be 
employed  as  one  of  a  group  of  symptoms  on  which  the  ultimate  opinion 
is  based. 

§  88.  What  is  the  pulse  ?— In  order  fully  to  appreciate  the  study 
of  the  arterial  pulse,  it  is  essential  to  have  a  proper  conception  of  the  true 
nature  of  what  it  is  we  perceive  when  we  examine  the  pulse  with  the  finger. 
Broadbent  ^^®  very  properly  calls  attention  to  a  universal  misconception  of 
what  the  pulse  is,  and  points  out  that  it  is  not  an  expansion  of  the  artery 
due  to  the  blood  discharged  into  the]aorta.    Marey  ^^^  says  that  the  expansion 


EXAMINATION  OF  THE  ARTERIAL  PULSE  91 

is  so  slight  that  many  physiologists  have  denied  its  existence,  and  he  states 
that  Poiseuille  has  demonstrated  that  in  the  larger  arteries  a  slight  expansion 
with  each  systole  does  take  place.  No  doubt  the  aorta  and  its  primary 
branches  are  somewhat  dilated  by  the  injected  blood,  but  whatever  the 
expansion  may  be  in  them,  in  the  carotid  and  radial  it  must  be  very  minute. 
To  feel  the  pulse  or  to  take  a  tracing,  it  is  necessary  that  the  artery  should 
be  flattened  against  the  bone.  Lister  states  that  it  is  for  this  reason  that 
surgeons  operating  in  close  proximity  to  a  large  artery  may  be  utterly  uncon- 
scious of  its  neighbourhood,  unless  they  inadvertently  wound  it  or  recognize 
its  pulsation  by  having  compressed  it  against  some  resistant  structure. 
The  visible  movements  of  the  artery  are  extremely  deceptive.  They  often 
give  the  appearance  of  contracting  and  expanding,  but  if  the  movement 
be  critically  examined,  it  will  be  found  to  be,  in  reality,  a  displacement  of 
the  artery.     A  straight  artery  like  the  carotid  resembles  somewhat  a  cord 


FiC4.  35.  The  upper  tracing  was  taken  with  the  receiver  over 
the  carotid  artery,  at  the  same  time  as  the  lower  one  was  taken 
with  the  receiver  placed  by  the  side  of  the  carotid  artery.  The 
lower  tracing  is  the  inverse  of  the  upper. 

that  is  periodically  tightened  and  slightly  relaxed.  During  the  systole  of 
the  ventricle,  the  carotid  is  straightened  and  tightened,  and  it  becomes 
slightly  relaxed  during  the  ventricular  diastole.  In  persons  with  thin  necks 
this  movement  can  be  studied.  If  we  place  one  receiver  over  the  carotid 
and  one  alongside  it,  and  have  the  movements  properly  registered,  the  one 
tracing  will  be  found  to  be  the  exact  reverse  of  the  other  (Fig.  35).  If  the 
artery  expanded  during  the  ventricular  systole,  it  would  naturally  thrust 
out  aU  the  tissues  surrounding  it,  and  the  tracing  from  the  side  would  then 
be  an  exact  duplicate  of  the  one  taken  from  the  front  of  the  artery.  The 
movement,  then,  of  the  beating  carotid  is  one  of  displacement  of  the  whole 
vessel,  not  a  dilatation  and  contraction  of  the  vessel. 

A  similar  confusion  arises  in  studying  an  artery  when  it  is  tortuous. 
In  looking  at  the  radial  when  it  is  tortuous,  one  can  readily  imagine  that  the 
rising  and  falling  of  the  artery  is  really  a  distension  and  contraction  of  the 
artery.  But  if  a  suitable  case  be  taken  where  in  the  course  of  the  tortuous 
artery  there  is  a  short  lateral  bend,  the  movement  can  be  demonstrated 


92 


DISEASES  OF  THE  HEART 


to  be  due  to  the  displacement  of  the  artery,  and  not  due  to  expansion  and 
contraction  of  the  artery.  If  the  pad  of  the  sphygmograph  spring  be  placed 
close  to  the  artery  on  the  concave  side  of  the  bend,  and  a  tracing  taken, 
it  will  be  found  that  during  the  ventricular  systole  the  bend  is  exaggerated, 
the  artery  being  pushed  farther  away  from  the  straight  course,  and  during 
ventricular  diastole  the  bend  diminishes.  If  tracings  be  taken  of  the  pulse 
in  such  a  radial  artery  at  the  same  time  as  the  carotid  pulse  (Fig.  36),  it  will 
be  found  that  the  radial  gives  an  inverted  tracing  comparable  to  that  in  the 
preceding  figure.  If  the  visible  movement  were  due  to  the  expansion  and 
contraction  of  the  artery,  the  lever  would,  on  the  contrary,  rise  during  systole 
and  fall  during  diastole,  as  in  an  ordinary  sphygmogram. 

What  we  recognize  then  as  the  pulse  is  the  sudden  increase  of  pressure 
within  the  artery  pressing  against  our  finger  when  we  compress  the  artery. 
With  the  cessation  of  the  ventricular  systole  the  resistance  to  our  finger 
steadily    diminishes    until    the    next    ventricular    systole    suddenly    rises. 


Fig.  36.  Simultaneous  tracings  of  the  carotid  and  radial  pulses.  The  radial  tracing  was 
taken  by  placing  the  pad  of  the  sphygmograph  by  the  concave  side  of  a  bend  of  the  tortuous 
radial  artery.  During  systole  the  artery  receded  from  the  sphygmograph  and  returned  during 
diastole,  and  hence  the  tracing  obtained  is  an  '  inverted  sphygmogram  '. 


Broadbent  ^^^  uses  the  folloAving  apposite  illustration  :  '  Such  a  pulsation  can 
be  felt  on  a  large  scale  by  placing  the  foot  on  the  inelastic  leather  hose  of  a 
fixe-engine  in  action,  in  which  there  can  be  no  expansion.' 

To  speak  of  the  pulse  as  being  the  expansion  and  contraction  of  the 
arterial  walls,  or  '  the  swinging  backwards  and  forwards  of  the  arterial  wall ', 
is  not  only  to  use  language  of  exaggeration,  but  to  convey  a  totally  erroneous 
conception  of  what  the  pulse  reaUy  is. 

§  89.  Inspection  of  the  arteries — Inspection  of  the  arteries  reveals 
in  health  but  little  movement.  Conditions  giving  rise  to  forcible  action  of 
the  left  ventricle  may  render  the  pulse  visible  in  some  of  the  superficial 
arteries.  Exertion,  excitement,  or  the  febrile  state  may  induce  visible 
beating  of  the  carotids,  while  this  is  a  marked  feature  when  the  arteries  are 
tortuous  and  atheromatous,  and  in  such  a  disease  as  exophthalmic  goitre. 
In  free  aortic  regurgitation,  not  only  is  there  marked  pulsation  of  the  carotids, 
but  pulsation  is  visible  in  numerous  superficial  arteries  in  various  situations. 


EXAMINATION  OF  THE  ARTERIAL  PULSE  93 

The  tortuous  character  of  superficial  arteries  is  visible  in  arterial  degene- 
ration. 

§  90.  Digital  examination  of  the  arteries — It  is  usual  in  the  routine 
examination  of  the  pulse  to  place  two  or  three  finger  tips  on  the  radial 
artery  near  the  Avrist.  The  fingers  are  laid  on  the  artery,  and  moved  upwards 
and  downwards  and  across  the  artery,  at  first  gently,  and  then  with  more 
pressure.  By  this  procedure  a  knowledge  of  the  size  of  the  artery  and  the 
conditions  of  its  walls  is  acquired.  Steady  pressure  being  applied  in  order 
to  obliterate  the  pulse,  the  force  required  to  attain  this  gives  an  idea  of 
the  arterial  pressure,  and  of  the  character  of  each  individual  pulse-wave. 
It  is  a  good  thing  to  practise  the  digital  examination  of  the  pulse  with 
sphygmographic  tracings  taken  at  the  same  time.  By  this  means,  the 
character  of  the  pulse  will  be  better  appreciated  by  the  finger. 

The  condition  of  the  walls. — We  recognize  the  yielding  nature  of  the 
arterial  coats  in  healthy  arteries.  In  degeneration  of  the  coats  the  arterial 
walls  may  be  universally  thickened,  or  contain  bead-like  patches  of  induration 
as  in  atheroma,  or  the  artery  may  have  become  a  rigid  tube  as  in  calcareous 
degeneration. 

The  size  of  the  artery. — The  variations  in  size  depend  entirely  upon 
the  degree  of  relaxation  of  the  muscular  coat  of  the  artery.  A  large  artery 
is  not  necessarily  significant  of  a  strong  pulse,  nor  a  small  artery  of  a  weak 
pulse.  An  increase  in  the  size  of  the  artery  frequently  implies  diminished 
opposition  to  the  work  of  the  heart.  The  size  of  the  artery  can  sometimes 
be  readily  appreciated  by  lightly  rolling  it  under  the  fingers.  At  other  times 
it  can  only  be  detected  when  the  pulse  is  elicited  by  firm  pressure  at  the 
place  where  we  expect  to  find  it.  This  difficulty  may  occur  where  there 
is  a  good-sized  artery  embedded  in  a  fat,  well-padded  wi'ist,  or  where  the 
artery  is  small  and  contracted.  On  the  subsidence  of  a  fever,  a  notable 
diminution  in  the  size  of  the  artery  can  often  be  readily  recognized. 

The  arterial  'pressure. — The  trained  finger  is  as  yet  the  best  guide  we 
have  in  judging  the  pressure  within  an  artery.  The  knowledge  necessary 
to  determine  what  is  normal  and  what  is  abnormal,  can  only  be  acquired 
by  the  constant  study  of  the  pulse.  The  finger  tips  become  so  educated 
in  course  of  time  that  we  readily  appreciate  the  sensation  conveyed  in 
compressing  an  artery  (see  Chapter  XII). 

The  pulse-rate. — The  reckoning  of  the  pulse-rate  should  be  made  at 
a  late  stage  in  the  examination.  When  abnormally  quicls,  it  should  be 
again  counted  when  the  patient  has  regained  his  composure.  It  is  best 
enumerated  in  two  separate  half-minutes,  to  ascertain  if  the  heart  is  acting 
quite  steadily.      In  children,  unless  asleep,  abnormal  frequency  is  often 


94  DISEASES  OF  THE  HEART 

very  unreliable  as  a  guide,  as  the  presence  of  the  doctor  often  keeps  up  a  con- 
tinued excitation  of  the  heart.  While  the  rate  of  the  pulse  normally  indicates 
the  number  of  the  contractions  of  the  left  ventricle,  it  sometimes  happens 
that  these  are  so  weak  that  some  of  the  pulse-waves  are  not  perceptible  to 
the  fingers.  In  such  cases  the  pulse  is  usually  slow  or  irregular  in  rhythm. 
To  appreciate  the  significance  of  the  pulse-rate,  due  regard  should  be  paid 
to  the  age  and  idiosyncrasies  of  the  patient,  and  to  the  ailment  from  which 
he  suffers. 

The  size  of  the  pulse-wave. — The  trained  finger  can  recognize  a  great 
variety  in  the  apparent  volume  of  the  wave  itself.  Some  waves  seem  to 
roU  up  under  the  finger,  passing  gradually  away,  while  others  pass  quickly, 
giving  a  mere  flick  to  the  finger. 

The  impact  of  the  pulse-ivave  on  the  finger. — This  may  be  quick  and 
abrupt,  and  the  pulse-wave  quickly  disappear  (pulsus  celer),  or  the  impact 
may  approach  the  finger  gradually  and  gradually  subside  (pulsus  tardus). 
Although  the  pulse-wave  occupies  such  a  short  space  of  time,  yet  the  sensitive 
finger  readily  recognizes  these  different  features. 

The  rhythm  of  the  pulse. — The  beats  usually  follow  one  another  at 
regular  intervals,  and  should  be  of  equal  strength.  The  divergencies  from 
the  normal  rhythm  are  numerous,  and  the  usual  terms  employed  to  distin- 
guish them  are,  in  my  opinion,  both  unsatisfactory  and  misleading,  but 
this  subject  is  fully  entered  into  later.  In  estimating  the  rhythm  of  the 
pulse,  one's  whole  attention  should  be  concentrated  upon  the  observation. 
If  one  does  not  exclude  other  thoughts  from  the  mind,  a  variation  in  the 
pulse  rate  and  strength  may  apparently  be  felt.  This  is  due  to  a  failure 
to  appreciate  the  pulse  during  a  remission  of  the  attention.  I  have  not 
only  been  conscious  of  this  myself,  but  in  cases  where  it  was  important  to 
note  the  fact,  as  in  pneumonia,  I  have  found  my  colleagues  describing 
irregularity  as  being  present,  when  careful  examination  revealed  a  perfectly 
regular  pulse. 

The  two  radial  jmlses  compared. — Finally,  the  two  radial  pulses  should 
be  compared,  and  any  difference  in  the  character  of  the  beats  noted. 
A  difference  in  the  strength  of  the  two  pulses  may  be  due  either  to  an 
abnormal  distribution  of  the  arteries  on  one  side,  or  to  an  interference  with 
the  lumen  of  a  vessel  on  one  side.  A  difference  in  the  character  of  the  pulse 
usually  occurs  only  in  the  latter  case.  The  two  most  frequent  conditions 
altering  the  character  of  the  pulse  on  one  side,  are  the  presence  of  an 
aneurysm  or  of  an  atheromatous  plate,  diminishing  the  lumen  of  the  vessel, 
on  the  proximal  side  of  the  place  where  the  pulse  is  examined. 

§  91.  The  value  of  a  sphygmogram — Although   the  sphygmogram 


EXA^IINATION  OF  THE  ARTERIAL  PULSE  95 

represents  the  variations  in  arterial  pressure,  and  although  it  can  give 
information  in  this  respect,  yet  there  are  so  many  sources  of  error,  that  it 
cannot  be  trusted  implicitly.  Its  greatest  service  is  in  giving  an  accurate 
record  of  the  movements  of  the  left  ventricle.  However  eloquent  may  be 
the  words  of  a  writer,  he  cannot  in  a  page  convey  as  clear  an  idea  of  the 
rhythm  of  a  heart  as  a  simple  pulse-tracing,  and  if  writers  had  given  us 
more  pulse-tracings  their  works  would  have  been  greatly  enhanced  in  value. 
It  is  because  it  gives  us  a  permanent  and  accurate  record,  that  a  tracing  of 
the  arterial  pulse  is  of  such  great  value.  When  we  seek  to  find  the  nature 
of  any  movement  of  the  circulation  by  recording  it  graphically,  the  arterial 
pulse  is  the  best  and  most  useful  standard  by  which  we  can  find  its  position 
in  the  cardiac  cycle,  as  will  be  shown  later. 

§  92.  Definition  of  a  sphygmogram. — When  the  spring  of  a  sphygmo- 
graph  is  so  accurately  adjusted  on  an  artery  that  it  does  not  obliterate 
the  artery  when  the  arterial  pressure  is  at  the  lowest,  and  still  slightly  com- 
presses the  artery  when  the  arterial  pressure  is  at  the  highest,  the  spring 
will  oscillate  with  each  variation  of  pressure  within  the  vessel.  This  oscil- 
lation being  communicated  to  the  lever  and  recorded  on  the  tracing-paper 
gives  us  a  series  of  wavy  lines,  which  represent  the  variations  of  the  pressure 
within  the  artery.  A  sphygmogram  may  therefore  be  defined  as  a  diagram- 
matic representation  of  the  variations  of  pressure  within  an  artery.  If 
we  knew  exactly  the  amount  of  pressure  exercised  by  the  spring,  we  should 
be  able  to  obtain  the  value  of  each  movement.  But  the  possibilities  of  error 
are  so  numerous  that  it  is  useless  to  draw  conclusions  from  the  amount  of 
pressure  supposed  to  be  exercised.  From  the  examination  of  a  tracing 
we  obtain  information  on  three  different  points  :  first,  concerning  the  rate 
and  rhythm  of  the  heart's  action  ;  second,  concerning  the  sequence  of  certain 
events  occurring  in  a  cardiac  revolution  ;  third,  concerning  the  character 
of  the  blood-pressure  within  the  artery. 

§  93.  Events  occurring  during  a  cardiac  revolution  revealed  by  the 
sphygmogram.  (a)  The  systolic  i:)eriod. — If  we  take  a  sphygmogram  we 
can  divide  the  cardiac  cycle  into  two  periods  :  one  {E,  Fig.  37)  during  which 
the  aortic  valves  are  open  and  the  ventricle  pours  its  contents  into  the  aorta, 
and  another  {G,  Fig.  37)  during  which  the  aortic  valves  are  closed  and  the 
ventricle  is  in  diastole.  For  the  sake  of  convenience  in  describing  sphygmo- 
grams  these  two  periods  \vill  be  referred  to  as  the  systolic  and  diastolic 
periods,  although  in  the  space  G  the  presphygmic  and  postsphygmic  periods 
of  the  ventricular  systole  are  included  (Fig.  43).  The  character  of  the  systolic 
portion  varies  very  much  in  different  individuals.  These  variations  depend 
mainly  on  the  amount  of  resistance  offered  by  the  arteries  to  the  ventricular 


96 


DISEASES  OF  THE  HEART 


systole.  In  such  a  tracing  as  Fig.  37  there  is  first  an  abrupt  rise  (p),  then 
a  faU  followed  by  a  continuation  of  the  wave  (s)  at  about  the  same  level. 
This  period  is  usually  described  as  being  divided  into  two,  the  abrupt  rise 
being  spoken  of  as  the  primary  or  percussion  wave,  and  the  latter  portion 
as  the  tidal  or  predicrotic  wave  (the  papillary  wave  and  outflow  remainder 
wave  of  Roy  and  Adami).  This  division  has  led  to  the  idea  that  these 
represent  two  different  events  in  the  pulse  itself.     As  a  matter  of  fact,  the 


Fig.  37.  Sphygmogram  of  the  radial  pulse.  The  space  E 
is  the  period  of  ventricular  systole  when  the  aortic  valves  are 
open  ;  the  space  G  the  period  of  ventricular  diastole  ;  s  is  the 
pulse-wave  due  to  the  ventricular  systole  ;  n  the  aortic  notch  ; 
d  the  dicrotic  wave  ;  and  p  a  wave  due  to  instrumental  defect. 

abrupt  rise  2^  above  the  level  of  the  wave  s  is  due  to  instrumental  defect, 
and  the  whole  period  E  is  occupied  by  the  ventricular  pressure  forcing  blood 
into  the  arterial  system,  and  corresponds  with  the  period  E  in  Fig.  43.  In 
cases  where  the  arterial  pressure  is  low  relatively  to  the  strength  of  the 
ventricular  systole,  these  two  waves  are  so  blended  together  that  so-called 
percussion  and  tidal  waves  can  no  longer  be  differentiated  (Fig.  38).  The 
whole  of  this  period  E  in  the  tracing  will  hereafter  be  referred  to  as  the 
systolic  period,  and  the  wave  s  as  the  systolic  wave,  as  it  represents  the 


Fig.  38.     The  letters  have  the  same  significance  as  in  Fig.  37. 

period  of  ventricular  systole  when  the  ventricle  and  arterial  system  are  in 
free  communication. 

(6)  The  diastolic  period. — With  the  closure  of  the  aortic  valves,  the 
arterial  pressure  faUs  rapidly  to  the  bottom  of  the  aortic  notch  7i  (Figs.  37 
and  38).  In  the  tracings  this  is  seen  to  be  at  the  beginning  of  the  diastolic 
period.  This  fall  is  interrupted  by  a  distinct  rise  in  the  pressure  represented 
by  the  dicrotic  wave  d.  There  has  been  a  good  deal  of  discussion  concerning 
the  cause  of  the  dicrotic  wave.  The  following  explanation  seems  to  me  the 
most  probable.      The  semilunar  valves  are  so  delicately  constructed  that 


EXAMINATION  OF  THE  ARTERIAL  PULSE 


97 


they  readily  respond  when  the  pressure  on  one  side  rises  above  that  on  the 
other.  As  soon  as  the  aortic  pressure  rises  above  the  ventricular  the  valves 
close.  At  the  moment  this  happens  the  valves  are  supported  by  the  hard, 
contracted  ventricular  walls.  The  withdrawal  of  the  support  by  the  sudden 
relaxation  of  these  walls  will  tend  to  produce  a  negative  pressure  wave  in 
the  arterial  system.  But  this  negative  wave  is  stopped  by  the  sudden 
stretching  of  the  aortic  valves,  which,  on  losing  their  firm  support,  have  now 


Fig.  39.  A  strong- beating  ventricle  has  jerked  tlie  lever  high  above  the  true  systolic  wave, 
and  the  falling  lever  has  made  an  artificial  notch  on  the  systolic  wave  s.  The  true  pulse  curve 
is  probably  represented  in  the  dotted  tracing. 

themselves  to  bear  the  resistance  of  the  arterial  pressure.  This  sudden 
checking  of  the  negative  wave  starts  a  second  positive  wave,  which  is  pro- 
pagated through  the  arterial  system  as  the  dicrotic  wave.  After  the  dicrotic 
wave  the  arterial  pressure-curve  gradually  falls.  Occasionally  there  are 
slight  waves  in  the  fall,  but  these  are  of  doubtful  import. 

§  94.  Features  of  the  sphygmogram  due  to  instrumental  defect. — 
In  the  study  of  sphygmographic  tracings  one  has  always  to  bear  in  mind  that 


Fig.  40.     The  forcible  changes  in  pressure  have  exaggerated  the  height  and  depth 

of  all  the  waves. 

certain  features  may  be  due  to  the  instrument  itself.  Speaking  generally, 
these  instrumental  features  occur  where  there  are  sudden  and  forcible 
changes  in  the  arterial  pressure.  The  most  frequent  of  these  is  the  jerking 
up  of  the  spring  by  the  systolic  wave  itself.  Then  the  next  most  frequent 
is  the  formation  of  a  notch  on  the  tracing  of  the  systolic  wave,  due  to  the 
sudden  fall  of  the  spring  after  being  jerked  high  up,  as  in  Fig.  39.  Occa- 
sionally one  finds  the  aortic  notch  artificially  deepened  by  the  sudden 
lowering  of  the  pressure,  as  in  Fig.  40. 

MACKENZIE  jj 


CHAPTER   XII 

Arterial  Pressure 

§  95.  The  cause  of  arterial  pressure. 

96.  Methods  of  measuring  the  blood-pressure. 

97.  Increased  blood-pressure. 

98.  Hyperpiesis. 

99.  Effect  on  the  heart  of  increased  peripheral  resistance. 

100.  Increased  arterial  pressure  and  heart  failure. 

101.  Treatment  of  high  arterial  pressure. 

102.  Diminished  arterial  pressure. 

§  95.  The  cause  of  arterial  pressure — When  the  left  ventricle 
contracts  it  drives  the  blood  into  the  arterial  system.  The  escape  through 
the  arterioles  and  capillaries  is  retarded,  so  that  the  blood  continues  to  flow 
after  the  ventricle  has  ceased  to  contract.  As  a  consequence  of  this,  the 
arteries  are  slightly  distended  during  ventricular  systole,  and  their  elastic 
coats  compress  the  column  of  blood  within  them  after  the  ventricular  systole 
is  over,  and  thus  maintain  a  degr.ee  of  arterial  pressure  during  the  period 
in  which  the  ventricle  is  not  acting.  The  ventricular  force  is  thus  stored  up 
by  the  distension  of  the  elastic  coats  of  the  arteries,  and  hberated  during 
the  ventricular  diastole. 

The  chief  factors  therefore  concerned  in  the  maintenance  of  arterial 
pressure  are  the  ventricular  systole,  the  peripheral  resistance,  and  the  elastic 
recoil  of  the  arteries.  The  viscosity  of  the  blood  is  also  a  factor  in  the 
raising  of  the  arterial  pressure. 

§  96.  Methods   of   measuring  the    blood-pressure Of  late  years 

many  instruments  have  been  devised  to  measure  the  arterial  pressure. 
The  majority  are  constructed  on  the  principle  of  compressing  the  brachial 
artery  with  an  air-bag  embracing  the  upper  arm.  Air  is  pumped  into  the 
bag,  and  its  pressure  is  measured  by  a  mercury  manometer  in  connexion 
with  it.  When  the  pressure  is  raised  sufficiently  to  obliterate  the  radial  pulse, 
we  obtain  the  only  really  trustworthy  standard,  and  it  is  this  I  refer  to  here- 
after as  '  arterial  or  blood  pressure  '.  Attempts  have  been  made  to  estimate 
the  systolic,  mean,  and  diastolic  pressures  by  observing  or  recording  the 
movements  communicated  to  the  column  of  mercury  by  the  compressed 
artery.  It  is  found  that,  during  the  gradual  compression  of  the  artery, 
oscillations  due  to  the  pulse  beat  occur  in  the  mercury.  These  oscillations 
begin,  gradually  reach  a  maximum,  and  gradually  decrease  as  the  pressure 


ARTERIAL  PRESSURE  99 

is  raised  or  lowered.  Far-reaching  deductions  have  been  drawn  from  the 
changes  in  these  oscillations.  I  think,  if  the  cause  of  these  oscillations  be 
properly  appreciated,  no  safe  deductions  can  be  drawn  as  to  what  is  called 
the  systolic,  mean,  or  diastoUc  pressures.  When  the  pressure  within  the 
air-bag  corresponds  to  that  of  the  artery,  the  arterial  pulse  communicates 
its  impact  to  the  air  in  the  bag,  and  thus  induces  the  oscillation  of  the 
mercurial  column.  The  size  of  these  oscillations  depends  on  the  amount 
of  movement  of  the  arterial  wall.  Let  the  Hnes,  A,  B,  Fig.  41,  represent  the 
walls  of  the  artery,  and  for  simpUcity  assume  that  the  pressure  is  applied 
to  one  side  only  of  the  vessel.  It  is  found  that  a  pressure  of  160  millimetres 
obliterates  the  arterial  pulse,  the  wall  A  being  flattened  down  on  B  with  such 
force  that  no  blood  passes  through,  and  there  is  no  oscillation  of  the  mercurial 


Fig.  41.  Diagram  to  show  the  nature  of  the  oscillations  of  the  mercurial  column  in  esti- 
mating the  blood-pressure.  A  and  B  represent  the  walls  of  the  brachial  artery.  At  160  the 
lumen  of  the  artery  is  obliterated  by  the  pressure  of  an  air-bag  embracing  the  upper  arm.  As 
the  pressure  is  gradually  lowered  in  the  bag,  each  beat  of  the  artery  produces  a  movement  of 
the  mercury  in  the  manometer,  the  movement  being  represented  by  the  elevations  in  the 
diagram.  With  diminution  of  pressure  there  is  at  first  a  gradual  increase  in  the  extent  of  the 
movement  followed  by  a  gradual  decrease  until  the  pressure  in  the  air-bag  ceases  to  compress 
the  artery.  From  this  it  is  shown  that  there  is  no  definite  period  which  can  be  said  to  corre- 
spond to  the  systolic,  diastolic,  or  mean  blood-pressure. 

column.  When  the  pressure  is  lowered  to  150,  a  small  wave  escapes  during 
systole  which  raises  the  wall  to  a  slight  extent,  and  gives  rise  to  a  small 
oscillation.  At  140  a  larger  wave  escapes,  but  the  pressure  of  140  is  still 
sufficient  during  a  portion  of  diastole  to  flatten  the  wall  A  against  B.  At 
130  the  pressure  no  longer  flattens  the  wall  A  against  B,  but  the  flow 
escapes  during  diastole,  and  the  oscillation  reaches  its  maximum.  With 
the  gradual  lowering  of  the  pressure,  the  maximum  oscillation  persists. 
At  110  the  artery  is  fully  distended  during  systole,  and  only  partially 
compressed  during  diastole,  but  the  pulsation  is  still  maximal.  As  the 
pressure  falls  there  is  a  decrease  in  the  compression  of  the  artery  and 
a  corresponding  decrease  in  the  size  of  the  oscillation,  until  the  pressure 
fails  to  compress  the  artery  sufficiently  to  produce  any  movement.  From 
this  way  of  looking  at  the  matter,  it  wiU  be  realized  that  at  no  definite  period 

h2 


100  DISEASES  OF  THE  HEART 

can  we  tell  when  the  record  represents  a  systolic,  a  mean,  or  a  diastolic  pres- 
sure, and  that  the  maximal  oscillation  may  last  through  a  considerable 
range  of  pressure  with  nothing  to  guide  one  to  the  moment  when  any  definite 
pressure  could  be  ascertained.  The  diagram  may  not  represent  the  condition 
of  affairs  in  every  case,  and  a  limited  usefulness  may  possibly  be  found  in 
noticing  the  period  of  maximal  oscillation  and  its  decline,  but  so  far,  I  think, 
no  very  reliable  conclusion  can  be  drawn. 

The  force  required  to  obliterate  the  pulsation  in  the  radial  artery  is  fairly 
easily  ascertained,  and  from  it  certain  limited  inferences  may  be  drawn. 
It  is  doubtful  if  it  represents  the  actual  arterial  pressure  within  the  artery, 
for  an  escape  can  take  place  imperceptible  to  the  finger,  and  certain  external 
conditions  may  affect  the  pressure.  It  is  usually  assumed,  for  instance, 
that  the  arterial  wall  and  its  coverings  offer  such  a  slight  resistance  as  to 
be  negligible.  Russell  ^^^  on  the  other  hand,  asserts  that  the  thickening  or 
contraction  of  the  artery  may  have  a  very  considerable  effect,  and  that 
thick,  sclerosed,  and  contracted  arteries  may  offer  such  resistance  that 
a  considerable  proportion  of  the  pressure  may  be  spent  in  overcoming  it, 
OUver  ^2  has  shown  that  the  pressure  obtained  by  instruments  may  vary  in 
different  arteries  in  the  same  individual,  while  L.  Hill's  observations ''^  show 
that  the  arterial  wall  can  have  only  a  very  slight  influence  in  the  instru- 
mental observation  of  the  blood-pressure. 

There  are  a  great  many  different  instruments  devised  to  take  the  arterial 
pressure.  Most  of  them  are  somewhat  cumbrous,  and  some  patients  resent 
the  disagreeable  sensation  produced  by  compressing  the  upper  arm.  Hence 
these  methods  are  not  likely  to  receive  that  general  application  which  the 
need  for  ascertaining  the  blood-pressure  requires.  L.  Hill  has  recently 
invented  an  extremely  simple  and  practical  method.  In  place  of  a  cuff 
surrounding  the  upper  arm,  he  uses  a  small  bag  which  is  compressed  over 
the  radial  artery  until  the  pulse  disappears  below  the  place  of  compression. 
The  bag  is  connected  with  a  very  simple  manometer,  which  can  be  carried 
in  the  waistcoat  pocket. 

Erlanger  ^*  and  Gibson  '^^  have  invented  methods  for  graphically  record- 
ing the  blood-pressure.  The  tracings  from  Gibson's  apparatus  seem  very 
instructive,  but  I  have  no  experience  in  the  use  of  his  apparatus. 

A  great  deal  has  been  written  about  blood-pressure  and  its  estimation 
in  practical  medicine,  but  it  must  be  confessed  that  much  of  it  has  been 
of  little  practical  value,  and  much  careful  observation,  extending  over  many 
years,  on  individual  patients,  will  be  necessary  before  any  sure  and  certain 
result  is  obtained.  The  remarks  I  make  on  the  subject  are  based  on  the 
examination  of  numerous  patients  in  the  endeavour  to  ascertain  some  sure 


ARTERIAL  PRESSURE  101 

foundation  on  which  to  base  the  application  of  the  method  in  the  chnical 
examination  of  heart  affection. 

§  97.  Increased  blood-pressure — In  many  cases,  one  can  corro- 
borate by  instrumental  observation  the  knowledge  previously  acquired  by 
the  finger,  that  the  pressure  in  the  arteries  increases  in  certain  diseased 
conditions,  as  Bright's  disease,  and  with  advancing  years.  As  the  increased 
pressure  of  advancing  years  is  associated  with  arterial  changes,  the  question 
of  cause  and  effect  is  a  very  difficult  one  to  solve.  On  the  one  hand,  the 
changes  in  the  blood-vessels  undoubtedly  tend  to  raise  the  blood-pressure, 
wliile  it  is  contended  that  these  are  induced  by  the  blood  itself  containing 
ingredients  that  provoke  a  contraction  of  the  arterioles,  in  consequence  of 
which  the  muscular  coat  hypertrophies.  A  rise  in  pressure  seems  to  induce 
atheromatous  degeneration,  and  this  in  turn  causes  a  rise  in  pressure,  and 
thus  a  vicious  circle  may  be  formed.  The  fact  is  undoubted,  that  arterial 
changes  and  high  blood-pressure  are  very  frequent  phenomena  in  advanced 
life.  The  changes  are  so  insidious  that  they  rarely  come  under  consideration 
until  they  are  well  established.  One  may  infer,  indeed,  that  such  changes 
are  occurring  in  middle  life,  when  one  notices  a  tortuous  temporal  artery, 
but  it  is  rare  that  the  condition  gives  any  cause  for  anxiety  until  it  is  well 
established. 

It  is  a  mistake,  and  one  made  not  infrequently,  to  begin  treating  the 
high  blood-pressure  as  if  it  were  a  disease.  Happily  the  efforts  employed 
to  reduce  the  blood-pressure  are  usually  of  little  value.  In  order  to  appre- 
ciate the  meaning  of  high  blood-pressure,  it  is  well  to  consider  the  condition 
associated  with  its  production,  for  I  think  it  has  a  significance  beyond  that 
of  being  a  manifestation  of  disease. 

I  have  already  pointed  out  that  the  arterial  pressure  is  maintained 
chiefly  by  the  force  of  the  left  ventricle,  the  peripheral  resistance,  and  the 
elastic  recoil  of  the  arteries.  The  necessity  for  the  pressure  is  the  regular 
and  equable  supply  of  blood  to  the  organs  and  tissues.  Between  the  heart 
and  tissues  there  is  an  intimate  association,  whereby  the  supply  to  the 
tissues  and  organs  is  moderated  by  their  requirements — the  heart  beating 
more  forcibly  and  more  rapidly,  and  the  peripheral  resistance  diminishing 
when  there  is  an  urgent  need,  by  the  exercise  of  the  functions  of  the  organs. 
With  advancing  age,  thi'ee  great  changes  occur  in  the  blood-vessels.  The 
elasticity  of  the  arteries  diminishes.  The  result  of  this  is  that  there  is  no 
longer  the  same  equable  maintenance  of  the  pressure  during  diastole.  The 
arteries  approximate  the  condition  of  rigid  tubes  where  the  force  exerted 
by  the  left  ventricle  is  not  sufficiently  stored  up  in  the  elastic  coats,  to  be 
liberated  during  diastole.     The  loss  of  this  assistance  necessitates  increased 


102  DISEASES  OF  THE  HEART 

force  of  the  ventricular  contraction,  and  therefore  an  increase  of  the  pressure 
during  ventricular  systole.  In  the  arterioles  there  may  be  an  increase  of 
the  muscular  tissue,  and  this  implies  an  increase  in  functional  activity 
with  an  increase  of  the  peripheral  resistance.  These  are  the  two  factors 
that  are  generally  assumed  to  be  the  cause  of  increased  blood-pressure, 
but  there  is  a  third  which  has  not  received  that  consideration  to  which  it  is 
entitled,  namely,  the  diminution  of  the  capillary  field.  This  can  be  recognized 
in  various  ways,  as,  for  instance,  the  thinning  and  wasting  of  the  skin  and 
subcutaneous  tissues,  and  by  the  absence  of  oozing  in  surgical  operations. 
The  manner  in  which  it  raises  the  blood-pressure  is  simply  by  narrowing 
the  passage  of  outflow  (see  §  221). 

§  98.  Hyperpiesis. — In  the  routine  examination  of  patients  we  meet 
occasionally  with  some,  usually  middle-aged,  sometimes  young,  who  show 
considerable  fluctuations  in  blood-pressure.  Periods  of  high  arterial  pressure 
(hyperpiesis  of  Clifford  Allbutt  ^^)  may  be  associated  with  some  discomfort, 
as  mental  dullness,  headache,  &c.  These  periods  can  be  cut  short  by  a  smart 
purge,  bodily  exercise,  &c.,  or  they  disappear  from  no  ascertainable  cause. 
It  is  possible  the  periods  of  high  arterial  pressure  are  due  to  faulty  metabolism, 
but  they  will  be  found  to  recur  in  spite  of  the  greatest  care  in  diet.  It  is 
said  by  some  that  these  periods  of  high  blood-pressure  are  the  cause  of 
arterial  degeneration,  but,  with  an  imperfect  knowledge  of  all  the  factois 
we  are  not  in  a  position  to  decide. 

§  99.  Effect  on  the  heart  of  increased  peripheral  resistance. — 
I  have  mentioned  that  the  connexion  between  the  heart  and  the  tissues  is  so 
intimate  that  the  demand  from  the  tissues  is  responded  to  by  stronger  con- 
traction of  the  heart.  When,  therefore,  one  or  all  of  these  causes  increasing 
the  peripheral  resistance  are  in  action,  the  heart,  in  order  to  supply  the 
tissues  with  blood,  has  to  exert  more  force  in  its  contraction.  It  accommo- 
dates itself  to  its  ever-increasing  burden  by  calling  upon  its  reserve,  and  the 
only  evidence  that  it  has  more  to  do  is  in  the  hmitation  of  its  field  of  response. 
One  can  almost  say,  when  an  individual  realizes  the  fact  that  a  hill  is  not 
climbed  with  the  ease  and  comfort  with  which  it  used  to  be  done,  that  already 
the  heart  is  meeting  an  increased  peripheral  resistance,  and  there  is  already 
a  slight  exhaustion  of  its  reserve  force.  This,  as  we  know,  is  a  very  gradual 
and  long-continued  process,  beginning  insidiously  in  the  fourth  decade  of 
life,  and  coinciding  with  the  time  at  which  athletes  abandon  the  exercises 
that  call  for  long  and  severe  exertion. 

As  the  changes  that  increase  the  peripheral  resistance  tend  slowly  but 
surely  to  advance,  the  work  of  the  heart  becomes  ever  greater,  the  field  of 
response  becomes  more  limited,  till  finally  the  patient's  attention  is  called 


I 


ARTERIAL  PRESSURE  103 

by  some  disagreeable  sensation  to  the  fact  of  the  great  limitation,  and  so 
we  get  heart  failure.  The  peculiar  feature  of  the  heart  failure  that  arises  in 
this  way  is,  that  the  function  of  the  heart  that  has  most  work  to  do  usually 
fails,  namely,  the  function  of  contractility,  so  that  it  is  in  these  cases  of 
high  arterial  pressure  that  we  meet  the  most  typical  symptoms  associated 
with  failure  of  the  function  of  contractility. 

But  this  is  not  all.  The  changes  that  have  taken  place  in  the  arterial 
walls  in  the  periphery  have  at  the  same  time  been  affecting  the  arteries 
of  the  heart,  with  the  result  that  the  muscle-fibres  are  imperfectly  nourished 
and  degenerate.  It  is  in  these  cases  of  long-standing  high  blood-pressure 
that  we  find  the  most  striking  evidence  of  degenerative  changes  in  the  heart 
muscle  associated  with  arterial  degeneration,  and  it  is  wonderful  how  long 
a  heart  extensively  degenerated  can  maintain  a  high  blood-pressure. 

Such  cases  of  degenerated  arteries  and  long-continued  high  blood-pressure 
end  by  a  degenerated  artery  giving  way  and  causing  cerebral  apoplexy, 
or  by  failure  of  the  heart.  The  latter  may  come  about  in  various  ways  :  by 
a  sudden  change  in  the  inception  of  the  heart's  contraction — for  it  is  in  these 
cases  we  frequently  find  the  extra-systole  and  nodal  rhythm — by  gradual 
exhaustion  of  the  contractihty,  often  with  angina  pectoris,  and  on  rare 
occasions  by  rupture  of  the  heart.  There  may  occur  a  somewhat  sudden  fall 
in  the  arterial  pressure  from  dilatation  of  the  heart.  When  this  occurs  there 
is  a  sudden  change  in  the  character  of  the  symptoms  which  I  have  given 
in  some  detail  in  the  chapter  on  dilatation  of  the  heart  (Chapter  XXIII). 

§  100.  Increased  arterial  pressure  and  heart  failure From  such 

considerations  it  will  be  realized  that  we  may  have  heart  failure  without 
fall  of  blood-pressure,  and  this  consideration  brings  clearly  into  view  the 
fact  that  heart  failure  in  these  cases  is  primarily  a  matter  of  exhaustion  of 
reserve  force.  In  cases  of  valvular  disease,  as  H.  Starling  ^'  points  out,  there 
may  be  marked  failure  of  the  heart  with  little  or  no  fall  in  blood-pressure, 
and  recovery  may  ensue  with  little  or  no  rise  in  blood-pressure.  It  will 
be  found,  however,  in  these  cases  that  the  heart  failure  is  not  associated 
with  a  loss  of  the  function  of  tonicity.  When  dilatation  occurs,  then  there 
is  usually  a  faU  of  blood-pressure,  and  recovery,  when  it  takes  place,  is 
accompanied  by  a  rise  of  blood-pressure. 

§101.  Treatment  of  high  arterial  pressure. — It  is  an  almost  universal 
custom  to  treat  the  signs  of  heart  failure  with  '  cardiac  tonics  '.  By  cardiac 
tonics  are  usually  meant  drugs  or  methods  that  are  supposed  to  raise  the 
blood-pressure.  Hence,  when  any  disorder  that  implies  inefficient  action 
of  the  heart  is  met,  such  drugs  as  digitaUs,  or  some  methods  of  exercise  and 
baths  supposed  to  raise  the  blood-pressure,  are  resorted  to.    It  is  manifest. 


104  DISEASES  OF  THE  HEART 

from  the  consideration  of  tlie  causes  that  induce  high  blood-pressure,  that_ 
this  treatment  is  iiuoiix'ct.  Happily  the  methods  and  drugs  have  far  less 
effect  than  is  supposed,  and  as  rest  is  usually  enjoined  at  the  same  time 
the  good  results  are  due  more  to  unconscious  adoption  of  the  best  principle 
of  treatment  than  to  the  efforts  that  are  supposed  to  be  remedial.  Manifestly, 
in  heart  failure  induced  or  aggravated  by  high  pressure,  the  best  line  of  treat- 
ment is  to  ease  the  load  and  give  the  heart  rest,  to  regain  some  store  of 
reserve  force.  Now  there  is  a  tendency  to  rush  to  the  opposite  extreme, 
and  to  endeavour  to  reduce  the  blood-pressure  by  administering  drugs  of 
the  vaso-dilator  class.  Luckily,  the  administration  of  these  drugs  is  of 
little  effect,  and  little  or  no  permanent  lowering  can  be  obtained  by  their 
use.  It  is  manifest  that  with  changed  arteries,  and  a  diminished  capillary 
outflow  through  obliteration  of  the  capillary  vessels,  a  high  blood-pressure 
is  necessary  to  supply  the  organism  with  blood.  If  it  were  possible  to 
reduce  the  blood-pressure  permanently  in  a  man  who  for  years  had  a  blood- 
pressure  of  180-200  mm.,  the  result  would  be  impaired  nutrition  of  the 
organism.  If  the  final  breakdown  of  these  patients  be  watched,  it  will  not 
infrequently  be  found  that  the  blood-pressure  does  fall  to  150  or  140  mm.  Hg., 
and  the  result  is  at  once  the  appearance  of  the  signs  of  extreme  heart  failure 
— dropsy,  enlarged  liver,  oedema  of  the  lungs,  &c.  So  serious  is  the  signifi- 
cance of  a  fall  of  blood-pressure  in  patients  with  cardio-sclerosis,  even  with  , 
attacks  of  angina  pectoris,  that  the  persistent  fall  of  pressure  is  an  evidence  I  ' 
of  the  final  exhaustion  of  the  heart,  though  the  anginal  attacks  may  cease.  ' 

The  principle  I  pursue  with  most  success  is  to  place  the  patient  under  l/ 
conditions  that  give  the  heart  less  work  to  do,  carefully  avoiding  '  cardiac  Ij 
tonics  '  and  '  vaso-dilators  ',  restricting  the  diet,  evacuating  the  bowels,  3,ndAfl 
permitting  such  exercise  as  the  patient  can  undertake  without  distress,'||     I 
according  to  the  lines  laid  down  in  the  chapter  on  treatment. 

§  102.  Diminished  arterial  pressure — The  question  of  low  pressure 
and  its  significance  is  an  extremely  puzzling  one.  Here  again  one  meets  the 
confident  assertion,  '  In  hypotonic  conditions  give  cardiac  stimulants  or 
vaso-constrictors.'  The  matter  is,  however,  far  more  complicated,  and 
I  am  only  dimly  groping  after  the  true  principles  of  treatment  in  these 
cases.  In  dilatation  of  the  heart,  as  best  seen  in  mitral  disease,  the  fall  of 
pressure  may  be  considerable,  and  the  administration  of  drugs  of  the 
digitalis  group  has  undoubtedly  a  most  beneficial  effect  in  improving  the 
patient's  condition,  and  in  raising  the  blood-pressure.  But  this  is  due  to 
the  special  effect  that  digitalis  has  upon  the  function  of  tonicity,  both  in  the 
heart  and  the  arterial  muscle-fibres.  But  in  low  pressure  associated  with 
other  conditions  the  drug  is  often  of  little  avail. 


CHAPTER   XIII 

The  Venous  Pulse 

§  103.  What  the  venous  pulse  shows. 

104.  Inspection  of  the  jugular  pulse. 

105.  Methods  of  recording  the  jugular  pulse. 

106.  The  recognition  of  the  events  in  a  jugular  pulse. 

107.  Description  of  the  events  in  a  cardiac  cycle. 

108.  The  causes  of  variation  of  pressure  in  the  auricle  and  in  the  jugular  vein. 

109.  Standards  for  interpreting  a  jugular  tracing. 

110.  The  carotid  wave. 

111.  The  notch  on  the  ventricular  wave. 

112.  The  diastolic  wave. 

113.  Changes  due  to  variation  in  the  rate  of  the  heart. 

114.  Method  of  analysing  a  tracing. 

115.  The  ventricular  form  of  the  venous  j^ulse. 

116.  Conditions  giving  rise  to  a  venous  pulse. 

§  103.  What  the  venous  pulse  shows. — The  consideration  of  the 
circulation  has  so  far  been  mainly  concerned  with  the  effects  of  the  contrac- 
tion of  the  left  ventricle.  When  the  apex  beat  is  studied,  or  the  characters 
of  the  arterial  pulse  analysed,  our  purview  is  limited  almost  entirely  to  the 
doings  of  the  left  ventricle.  The  arterial  pulse  indeed  gives  us  a  direct 
knowledge  of  the  left  ventricle's  action  during  but  a  portion  of  the  cardiac 
cycle,  namely,  during  the  period  when  the  aortic  valves  are  open.  When 
they  are  closed,  we  are  no  longer  directly  cognizant  of  what  is  happening 
in  the  left  ventricle.  We  come  now  to  the  study  of  a  subject  which  gives 
far  more  information  of  what  is  actually  going  on  within  the  chambers  of 
the  heart.  In  the  venous  pulse  we  have  often  the  direct  means  of  observing 
the  effects  of  the  systole  and  diastole  of  the  right  auricle,  and  of  the  systole 
and  diastole  of  the  right  ventricle.  The  venous  pulse  therefore  presents 
a  greater  variety  of  features,  and  may  manifest  variations  due  to  disease 
which  the  study  of  the  arterial  pulse  fails  to  reveal. 

§  104.  Inspection  of  the  jugular  pulse — In  examining  a  patient  for 
pulsation  in  the  jugular  vein,  it  is  generally  best  that  he  should  lie  down, 
though  in  some  rare  cases,  where  the  veins  are  greatly  distended,  the  pulsa- 
tion can  only  be  recognized  when  the  patient  sits  up.  The  pulsation  is 
most  commonly  limited  to  the  internal  jugular  veins,  and  these  veins,  lying 


106  DISEASES  OF  THE  HEART 

alongside  the  carotid  arteries,  are  never  visible,  being  covered  at  the  root 
of  the  neck  not  only  by  the  skin  and  sterno-mastoid  muscle,  but  by  a  variable 
quantity  of  adipose  tissue  ;  one  therefore  recognizes  the  venous  pulse  only 
by  the  character  of  the  movements  communicated  to  the  structures  covering 
the  vein.  In  that  form  of  the  venous  pulse  in  which  the  principal  wave  is  due 
to  the  auricular  systole,  the  sudden  collapse  of  the  tissues  covering  the  vein 
is  more  striking  than  the  protrusion.  If  one  further  carefully  times  this 
coUapse,  it  will  be  found  to  be  synchronous  with  the  arterial  pulse.  The  pulse 
in  the  internal  jugular  vein  is  often  mistaken,  even  by  experienced  observers, 
for  *  beating  of  the  carotids  '.  But  the  carotid  pulse  is  always  abrupt  and 
sudden  in  its  protrusion  of  the  covering  tissues,  and  gradual  in  the  shrinking. 
Furthermore,  when  one  finds  a  small  radial  pulse  and  a  large  pulsation  in 
the  neck,  one  may  safely  conclude  that  the  neck  pulsation  cannot  be  carotid, 
unless  under  very  exceptional  circumstances  (as  aneurysm).  When  the 
pulsation  is  in  the  more  superficial  veins,  as  the  external  jugular,  facial, 
or  superficial  thoracic  veins,  the  collapse  of  the  vein  synchronous  with  the 
carotid  pulse  is  usually  easy  of  recognition.  In  another  form  of  venous 
pulse,  where  the  pulsation  is  due  to  the  ventricular  systole,  the  engorge- 
ment of  the  veins  is  usually  so  great,  the  arterial  pulse  so  small,  and  the 
cardiac  mischief  so  evident,  that  the  recognition  of  the  venous  pulse  is 
comparatively  easy. 

§  105.  Methods  of  recording  the  jugular  pulse Usually  the  move- 
ments of  the  vein  are  best  recorded  with  the  patient  lying  down,  the  shoulders 
slightly  raised,  the  head  comfortably  supported  by  a  pillow,  and  turned 
shghtly  to  the  right  in  order  to  relax  the  right  sterno-mastoid  muscle.  The 
receiver  [E,  Figs.  13,  p.  68,  and  18,  p.  73)  is  placed  over  the  jugular  bulb 
immediately  above  the  inner  end  of  the  right  clavicle,  with  just  sufficient 
pressure  to  shut  off  the  interior  of  the  receiver  from  the  outer  air.  One  may 
have  to  shift  the  receiver  about  to  get  the  best  movement.  The  relation 
of  the  jugular  bulb  to  the  surrounding  structures  is  shown  in  Fig.  42,  where 
the  circle  above  the  clavicle  indicates  the  position  of  the  receiver. 

Sometimes  better  tracings  are  got  higher  up  in  the  neck  or  from  the  left 
side.  In  great  engorgement  of  the  veins  it  may  be  possible  only  to  get 
a  tracing  when  the  patient  is  sitting  up.  The  continued  action  of  the 
sterno-mastoid  in  laboured  breathing  may  prevent  a  tracing  of  the  jugular 
pulse  being  obtained. 

§  106.   The  recognition  of  the  events  in  a  jugular  pulse There 

is  still  much  that  is  obscure  about  some  of  the  details  of  the  venous  pulse, 
and  several  of  these  are  still  the  subject  of  controversy.  In  the  following 
interpretation  I  deal  with  the  salient  points  which  have  thrown  most  light 


THE  VENOUS  PULSE 


107 


upon  the  obscure  features  of  the  heart's  action.  The  movements  of  the 
venous  pulse  are  usually  more  numerous  than  those  of  the  arterial,  and  in 
the  tracings  a  number  of  waves  are  present.  As  each  of  these  indicates 
a  rise  of  pressure  in  the  veins,  the  tracing  can  only  be  properly  interpreted 
when  the  force  producing  each  rise  of  pressure  is  known  ;  and  for  this 
purpose  the  time  of  appearance  of  each  wave  in  the  cardiac  cycle  must  be 


R  ^  inaomiaate  veia 


Fig.  42.  Shows  the  relation  of  the  internal  jugular  vein  to  the  carotid  and  subclavian 
arteries,  and  to  the  sterno -mastoid  muscle.  The  circle  represents  the  position  of  the  receiver  in 
taking  a  tracing.     The  spot  at  a  is  one  inch  from  the  internal  end  of  the  clavicle.     (Keith.) 

established.  This  is  done  by  taking  tracings  of  the  venous  pulse,  at  the 
same  time  as  some  movement  whose  position  in  the  cardiac  cycle  is  definite, 
and  the  arterial  pulse,  carotid  or  radial,  is  the  most  reliable.  The  apex 
beat  is  often  useful  and  convenient,  but  care  is  necessary  in  the  employment 
of  the  apex  beat,  as  has  already  been  pointed  out  (§  84). 

§  107.  Description  of  the  events  in  a  cardiac  cycle — In  the  diagram 
(Fig.  43)  there  is  represented  a  series  of  movements  due  to  various  forces 


108 


DISEASES  OF  THE  HEART 


that  occur  during  one  cardiac  cycle.  If  a  wave  be  found  in  the  vein,  and  if 
its  time  of  occurrence  be  ascertained  by  referring  to  the  place  it  would 
occupy  in  this  diagram,  we  can  usually  find  its  cause  by  noting  what  force 
is  operative  at  that  period.  It  must  be  added  that  while  this  diagram  repre- 
sents with  fair  accuracy  the  chief  events  in  a  cardiac  revolution,  it  is 
not  asserted  that  it  is  correct  in  every  detail.     Authorities  are  not  quite 


Fig.  43.  Semi-diagrammatic  representation  of  the 
auricular,  ventricular,  and  aoi-tic  pressures  during  one 
cardiac  revolution.  D,  the  presphygmic  period  of  the 
ventricular  systole  ;  E,  the  sjihygmic  or  pulse  period  ; 
F,  the  postsphygmic  period.  The  figures  1,  2,  3,  5,  and  6 
have  the  same  significance  as  those  in  Fig.  46.  The 
divisions  on  the  bottom  line  represent  tenths  of  a  second. 
(After  Frey.) 

agreed  on  several  smaU  points,  but  it  is  sufficient  for  the  purpose  I  have 
in  view. 

What  we  have  here  presented  are,  the  curves  representing  the  variations 
of  (1)  the  pressure  within  the  auricle  ;  (2)  the  pressure  within  the  ventricle  ; 
(3)  the  pressure  within  the  aorta.  The  spaces  embraced  by  the  perpendicular 
lines  represent  respectively  the  time  during  which  the  semilunar  valves  are 
open  [E)  and  the  auriculo-ventricular  valves  are  shut  {D,  E,  F).     I  would 


THE  VENOUS  PULSE 


109 


direct  attention  to  the  presphygmic  period  D,  when  the  ventricular  pressure 
is  rising,  but  has  not  yet  opened  the  aortic  valves  ;  and  to  the  postsphygmic 
period  F,  where  the  ventricular  pressure  is  falhng  after  the  closure  of  the 
aortic  valves.  The  curves  indicating  the  pressures  are  approximately 
correct,  but  are  utilized  here  to  show  the  periods  when  variations  take  place 
in  the  pressure.  Though  the  events  in  the  diagram  represent  what  happens 
in  the  left  side  of  the  heart,  there  can  be  no  doubt  that  the  changes  on  the 
right  side  are  of  the  same  character. 

§  1 08.  The  causes  of  the  variation  of  pressure  in  the  auricle  and 
in  the  jugular  vein.— The  auricular  pressure  in  Fig.  43  shows  a  series  of 
rises  and  falls,  and  these  correspond  to  those  in  a  venous  pulse  (Fig.  44), 
The  forces  operative  in  producing  the  variations  in  the  auricular  pressure 


Fig.  44.  Simultaneous  tracings  of  the  jugular  and  radial  pulses  and  of  the  carotid  and 
radial.  The  elevations  a  and  v,  and  falls  x  and  y  in  the  jugular  tracing  correspond  to  those 
in  the  auricular  pressure-curve  in  Fig.  43. 

are  also  acting  in  producing  the  jugular  pulse.  (The  curves  of  auricular 
pressure  by  different  physiologists  are  very  perplexing,  some  getting  a 
rise  of  varying  duration  during  ventricular  systole.  I  select  Frey's  as  the 
simplest  and  probably  the  truest.) 

The  auricular  ivave  (a)  and  fall  {x). — The  rise  a  in  the  jugular  pulse,  Fig.  44, 
corresponds  with  the  first  abrupt  rise  a  in  the  auricular  pressure-curve, 
Fig.  43,  and  both  are  due  to  the  systole  of  the  auricle.  Neglecting  the  wave  c 
for  discussion  later,  the  fall  x  in  the  jugular  pulse  corresponds  to  the  fall  x 
in  the  auricular  pressure-curve,  and  occurs  at  the  time  the  ventricle  is  in 
systole.  The  fall  is  due  to  three  factors  :  (1)  the  relaxation  of  the  auricle 
after  its  systole  ;  (2)  the  dragging  down  of  the  a. -v.  septum  by  the  ventricular 
muscle,  enlarging  the  auricular  cavity  as  described  in  §  20,  and  Fig.  3  ; 
(3)  the  diminished  intrathoracic  pressure  in  consequence  of  the  expul- 
sion from  the  chest  of  the  contents  of  the  left  ventricle.  When  there  is  a 
delay  in  the  ventricular  contraction,  the  factors  may  l)e  separated  as  in 


110 


DISEASES  OF  THE  HEART 


Fig.   112,  p.  177,  where  x  is  due  to  the  first  factor,  and  x'  to  the  second 
and  third  factors. 

The  ventricular  wave  {v). — The  rise  v,  after  the  fall  x  (Fig.  44),  is  due 
to  the  storing  of  blood  in  the  auricle  during  the  time  of  the  ventricular 
systole,  and  corresponds  with  the  second  rise  {v)  in  auricular  pressure-curve 
in  Fig.  43.  The  termination  of  this  rise  in  both  figures  is  sudden,  and  due 
to  the  opening  of  the  auriculo-ventricular  valves.  While  the  beginning  of 
this  rise  is  very  variable,  its  termination  is  one  of  the  most  certain  periods  in 
the  cardiac  cycle,  indicating  as  it  does  the  time  of  the  opening  of  the  tricuspid 
valves.  The  variableness  in  its  beginning  is  due  to  the  fact  that  it  owes  its 
origin  to  the  quantity  of  blood  stored  in  the  auricle  during  ventricular 
systole,  and  this  varies  in  individual  cases,  and  also  in  the  same  individual. 


Fig.  45.  Simultaneous  tracings  of  the  jugular  and  carotid  pulses,  showing  that  the  waves 
in  the  jugular  correspond  in  time  with  the  waves  of  increased  auricular  pressure  in  Fig.  43. 
In  this  patient  the  tricuspid  valves  were  partially  destroyed  and  the  orifice  therefore  markedly 
incompetent,  so  that  there  was  free  tricuspid  regurgitation.  The  wave  v  is  therefore  partly 
due  to  blood  regurgitating  from  the  right  ventricle. 

with  exertion  and  respiration.  The  blood  comes  mainly  from  the  periphery, 
pouring  into  the  auricles  through  the  veins.  When  the  auricle  becomes  filled, 
the  surplus  distends  the  superior  vena  cava  and  jugular,  and  hence  appears 
in  the  tracing  as  a  wave.  Another  source  is  sometimes  regurgitation  through 
the  tricuspid  orifice  (see  §  212).  It  is  necessary  to  bear  this  in  mind,  as  the 
failure  to  recognize  how  tricuspid  regurgitation  would  be  manifested  in  the 
venous  tracing  has  led  to  a  total  misconception  of  the  meaning  and  nature 
of  the  ventricular  form  of  the  venous  pulse.  It  has  been  assumed  that  in 
tricuspid  regurgitation  the  blood  sent  back  into  the  veins  would  appear  in 
the  jugular  at  the  same  time  as  in  the  carotid.  In  this  assumption  the  effects 
of  a  dilating  auricle  between  the  ventricle  and  veins  has  been  overlooked  ; 
as  a  matter  of  fact,  what  happens  is  merely  an  increase  in  the  amount  of 
blood  accumulating  in  the  auricle  during  the  ventricular  systole,  and  this 
causes  the  appearance  of  the  wave  v  to  be  somewhat  premature.  Thus,  for 
instance.  Fig.  45  is  from  a  case  where  there  was  a  damaged  tricuspid  valve. 


THE  VENOUS  PULSE 


111 


so  that  regurgitation  took  place,  and  the  wave  v  is  seen  to  be  of  small  size, 
beginning  early  in  the  time  of  the  ventricular  systole  (period  E). 

I  call  this  wave  {v)  the  ventricular  wave,  because  of  its  association  with 
the  systole  of  the  right  ventricle.  Thus  the  termination  of  the  wave  is  due 
to  the  relaxation  of  the  right  ventricle  and  opening  of  the  tricuspid  valves  ; 
it  is  often  made  up  of  blood  sent  back  through  the  incompetent  tricuspid 
orifice  by  the  systole  of  the  right  ventricle  ;  though  this  wave  may  be  small 
and  of  brief  duration  in  the  auricular  form  of  the  venous  pulse,  it  becomes 
increased  in  size  and  the  main  or  only  wave  in  the  ventricular  form  of  the 
venous  pulse. 


Fig.  46.  Tracings  of  the  jugular  pulse,  apex  beat,  carotid  and  radial 
pulses.  The  perpendicular  lines  represent  the  time  of  the  following  events  : 
1,  the  beginning  of  the  auricular  systole ;  2,  the  beginning  of  ventricular 
systole  ;  3,  the  appearance  of  the  pulse  in  the  carotid  ;  4,  the  appearance 
of  the  pulse  in  the  radial ;  5,  the  closing  of  the  semilunar  valves  ;  6,  the 
opening  of  the  tricuspid  valves  (compare  with  Fig.  43). 


The  fall  (y)  in  Figs,  43  and  44  is  due  to  the  blood,  that  has  been  stored 
in  the  auricle  during  ventricular  systole,  flowing  into  the  ventricle  after 
the  opening  of  the  tricuspid  valves.  Then  as  the  ventricle  becomes  filled, 
stasis  in  the  auricle  and  veins  takes  place,  causing  the  rise  between  y  and  a, 
Figs.  43  and  44,  till  the  auricle  again  contracts. 

§  109.  Standards  for  interpreting  a  jugular  pulse Such  are  briefly 

the  main  factors  concerned  in  the  production  of  the  auricular  form  of  the 
venous  pulse.  It  is  at  times  difficult  to  interpret  the  tracings,  so  that  it  is 
necessary  to  have  definite  standards  to  help  in  deciphering  certain  obscure 
features. 

In  Fig,  46  I  have  placed  below  the  jugular  pulse,  tracings  representing 
the  apex  beat  and  the  carotid  and  radial  pulses,  to  show  the  relation  in  time 
of  certain  events  in  these  various  movements.     The  numbered  perpendicular 


112 


DISEASES  OF  THE  HEART 


lines  indicate  the  simultaneous  events  in  the  jugular  pulse,  the  apex  beat, 
the  carotid,  and  the  radial  pulse.  The  perpendicular  lines  facilitate  the 
comparison  of  the  tracings  at  definite  points  in  the  cycle,  and  have  the 
same  significance  in  the  later  tracings  :  1,  the  beginning  of  the  auricular 
systole  ;  2,  the  beginning  of  the  ventricular  systole  ;  3,  the  opening  of 
the  semilunar  valves  and  the  appearance  of  the  carotid  pulse  ;  4,  the 
beginning  of  the  radial  pulse  ;  5,  the  closing  of  the  semilunar  valves  ; 
and  6,  the  opening  of  the  tricuspid  valves.  The  time  is  recorded  in  fifths 
of  seconds  in  this  and  other  tracings. 

Although  the  carotid  pulse  and  the  apex  beat  can  sometimes  be  usefully 
employed  as  a  standard,  it  will  be  found  that  the  radial  pulse  is,  on  the  whole, 


Fig.  47.  Simultaneous  tracings  of  the  jugular  and  the  radial  pulses  in  the  first  part  of  the 
tracing  and  of  the  carotid  and  the  radial  in  the  latter  part.  The  jugular  pulse  is  of  the  auricular 
type,  a,  auricular  wave  ;  c,  the  carotid  wave  ;  v,  the  ventricular  wave  ;  x,  the  auricular 
depression  ;  y,  the  ventricular  depression.  These  letters  have  the  same  significance  in  all 
the  other  tracings,  and  the  numbered  perpendicular  lines  have  the  same  significance  as  those 
in  Fig.  46. 

the  most  convenient  in  practice.  A  certain  loss  of  time  takes  place  in  the 
transmission  of  the  wave  to  the  radial  pulse,  and  this  can  be  estimated  by 
taking  simultaneously  with  the  radial  a  few  beats  of  the  carotid,  as  in  Figs. 
44  and  47,  in  which  the  space  between  3  and  4  shows  the  loss  of  time  between 
the  appearance  of  the  carotid  and  the  radial  pulse.  This  loss  being  allowed 
for,  one  can  always  find  a  definite  period  in  a  jugular  tracing  which  corre- 
sponds to  any  event  occurring  in  the  neck  due  to  the  ventricular  systole. 
T  also  employ  a  very  useful  period,  namely,  that  portion  of  the  ventricular 
systole  during  which  the  semilunar  valves  are  open  (period  marked  E  in 
all  the  tracings).  Its  duration  can  be  found  in  the  radial  tracing,  extending 
from  the  beginning  of  the  upstroke  to  near  the  bottom  of  the  dicrotic  notch. 
It  corresponds  to  the  time  between  the  perpendiculars  3  and  5  in  all  the  caro- 
tid, jugular,  and  apex  tracings  given  here.    In  the  neck  the  period  E  begins 


THE  VENOUS  PULSE 


113 


with  the  carotid  pulse.  There  is  a  slight  delay  between  the  opening  of  the 
aortic  valves  and  the  carotid  pulse,  but  it  is  so  short  (one-fiftieth  of  a  second) 
that  it  may  be  ignored.  The  space  E  in  the  radial  tracing  begins  about 
one-tenth  of  a  second  behind  the  same  period  in  the  neck. 

Another  important  standard  is  that  of  the  opening  of  the  tricuspid 
valves  (perpendicular  6  in  all  the  tracings),  which  in  jugular  tracings  is  always 
indicated  by  the  beginning  of  the  fall  of  the  wave  v.  In  the  apex  tracing 
this  event  occurs  at  the  bottom  of  the  fall,  after  the  systolic  plateau,  as  in 
Fig.  25. 

§  no.  The  carotid  wave — In  the  tracing  in  Figs.  44  and  47,  in  addi- 
tion to  the  waves  a  and  v,  which  have  already  been  described,  there  is  another 
wave  marked  c.  In  Fig.  42  it  will  be  seen  that  the  subclavian  and  carotid 
arteries  lie  in  such  close  proximity  to  the  jugular  vein  that  the  receiver 


Fig.  48.     Shows  a  diastolic  wave  h  in  the  jugular  tracing.     Rate  48. 

covers  a  portion  of  these  arteries.  In  consequence  of  this,  the  stroke  of 
the  arterial  pulse  affects  the  tracing  from  the  jugular,  and  produces  the  wave 
c,  which  I  have  caUed  the  carotid  wave.  A' considerable  amount  of  discussion 
has  taken  place  in  regard  to  the  cause  of  c,  but  if  an  observer  will  carefully 
take  tracings  higher  and  higher  up  in  the  neck,  he  can  easily  satisfy  himself 
of  its  nature,  for  it  gradually  assumes  the  character  of  a  tracing  from  the 
carotid  artery.  The  recognition  of  c  as  due  to  the  carotid  (or  carotid  and 
subclavian)  helps  much  in  the  analysis  of  tracings  from  the  neck,  particularly 
when  there  is  a  delay  between  the  auricular  and  ventricular  systole,  the  dura- 
tion of  the  a-c  interval  being  the  best  measure  of  the  delay.  (Experimental 
observations  show  that  faint  waves  may  occur  in  the  veins  about  the  time 
of  the  carotid  wave,  produced  in  some  obscure  way  by  the  systole  of  the 
ventricle,  but  the  carotid  and  subclavian  impact  is  the  main,  and  for 
practical  purposes  the  only  one,  that  need  be  considered.) 

The  true  venous  curve  would  follow  the  dotted  line  in  Figs.  46  and  47. 

UACEBNZIE  J 


114 


DISEASES  OF  THE  HEART 


§  III.  The  notch  on  the  ventricular  wave. — In  a  great  many  cases 
the  wave  v  has  a  notch  on  it  just  before  its  termination  (perpendicular 
line  5  in  Fig.  44).  It  corresponds  in  time  to  the  closure  of  the  semilunar 
valves,  and  the  following  rise  in  v  occurs  between  the  closure  of  the  semi- 
lunar valves  and  the  opening  of  the  tricuspid  valves  (postsphygrriic  interval, 


o-C.  "C  '^'^ 


a  c  ^     i  d    a  c 


v/  V  .        V 


Fig.  49.     In  increase  of  the  heart's  rate  the  period  between  y  and  a  becomes  shortened,  so 
that  the  auricular  wave,  a,  follows  immediately  after  v  (compare  with  Figs.  47  and  48)[. 

F,  Fig.  43),  The  exact  cause  of  this  notch  is  still  a  matter  of  dispute — 
no  satisfactory  explanation  being  yet  forthcoming.  I  have  often  employed 
it  as  a  useful  guide  in  measuring  the  period  when  the  semilunar  valves 
close,  and  it  is  represented  by  the  perpendicular  line  5  in  all  the  tracings. 


Fig.  50.     With  gi'eat  increase  in  the  rate  the  waves  v 
and  a  become  blended. 


§  112.  The  diastolic  wave — Occasionally  a  wave  may  be  detected  in 
slow-acting  hearts  shortly  after  the  opening  of  the  tricuspid  valves  {h,  Fig. 
48).  A.  G.  Gibson  '^''^  and  Hirschfelder  '^^^  describe  this  as  due  to  the  inrush 
of  blood  into  the  ventricle  floating  up  the  cusps  and  causing  a  transient 
closure  of  the  tricuspid  valves.  Thayer*"^  and  Gibson  also  describe 
a  sound  heard  occasionally  at  this  time. 


;     THE  VENOUS  PULSE  115 

§  113.  Changes  due  to  variation  in  the  rate  of  the  heart When 

the  heart's  rate  increases  the  shortening  of  the  cycle  takes  place  mainly 
at  the  expense  of  the  diastolic  period.  In  the  venous  tracing  the  first 
effect  is  shown  by  the  disappearance  of  the  period  of  stasis,  the  wave  a 
following  immediately  on  the  ventricular  wave  v  (Fig,  49)  ;  with  still  greater 
increase  in  the  rate,  v  and  a  become  blended  (Fig.  50). 


Tig.  51.     In  tracings  from  the  neck  the  small  wave,  a,  due  to  the 
auricular  systole  may  be  the  only  evidence  of  the  jugular  pulse. 

§  114.  Method  of  analysing  a  tracing.— In  the  tracings  given  so  far 
the  waves  have  been  distinct  and  well  marked.  It  often  happens  that  the 
jugular  pulse  is  extremely  small,  so  that  we  only  get  a  slight  movement 
due  to  the  auricle,  the  main  portion  of  the  tracing  being  due  to  the  carotid, 


Fig.  52.    The  movements  in  the  neck  seemed  dancing  vibrations  but  an  analysis  of  a  tracing 
refers  each  movement  to  a  definite  cause. 

as  in  Fig.  51.  At  other  times  the  movements  of  the  neck  seem  mere  dancing 
vibrations,  and  the  record  obtainable  shows  a  series  of  small  undulations. 
But  with  the  radial  pulse  as  a  standard,  one  can  definitely  assign  each 
undulation  to  the  force  producing  it.  Thus  in  Fig.  52  we  can  analyse  the 
tracing  by  the  following  procedure  :  Make  a  downstroke  (4)  parallel  with  the 
perpendicular  line  at  the  beginning  of  the  radial  tracing,  at  the  beginning  of 
a  radial  pulse  beat.     As  the  carotid  pulse  occurs  nearly  one-tenth  of  a  second 

I  2 


116  DISEASES  OF  THE  HEART 

before  the  radial,  draw  the  perpendicular  line  3  one-tenth  of  a  second  in 
front  of  4.  Measure  the  distance  from  the  perpendicular  line  at  the  beginning 
of  the  tracing  to  3.  Draw  a  downstroke  in  the  jugular  tracing  at  the  same 
distance  from  the  one  at  the  beginning.  This  will  be  found  to  fall  at  the 
beginning  of  a  small  wave,  which  therefore  must  have  been  due  to  the 
carotid,  and  so  mark  it  c.  The  auricular  wave  occurs  one-fifth  of  a  second 
in  front  of  c,  and  so  the  wave  a  can  only  be  due  to  the  auricular  systole. 
In  Fig.  46,  p.  Ill,  it  was  shown  that  the  opening  of  the  tricuspid  valves 
(perpendicular  line  6)  often  coincides  with  the  bottom  of  the  dicrotic  notch 
in  the  radial  tracing.     If  now  a  perpendicular  line  (6)  be  drawn  at  this 


Fig.  53.  Simultaneous  tracings  of  the  jugular  and  carotid  pulses,  showing  one  large  wave 
V,  synchronous  with  the  carotid  pulse,  and  due  to  the  ventricular  systole,  and  one  large  fall,  y, 
synchronous  with  and  due  to  the  ventricular  diastole.  There  is  no  sign  of  an  auricular  wave, 
and  the  jugular  pulse  is  therefore  of  the  ventricular  type,  and  the  rhythm  of  the  heart  is 
continuously  irregular. 

period  in  the  jugular  tracing,  it  wiU  be  found  to  faU  at  the  end  of  a  wave,  v, 
which  must  therefore  be  the  ventricular  wave. 

By  strictly  following  such  a  method  as  the  foregoing,  httle  difficulty  will 
be  experienced  in  analysing  the  great  majority  of  tracings, 

§  115.  The  ventricular  form  of  the  venous  pulse In  Figs.  53  and 

54  are  tracings  of  the  jugular  pulse.  At  a  glance  these  are  recognized  to  be 
totally  different  from  the  form  of  the  venous  pulse  just  described.  The 
waves,  V,  in  Figs.  53  and  54  are  due  to  the  blood  being  forced  back 
through  the  tricuspid  orifice  into  the  veins  by  the  contraction  of  the  right 
ventricle.  In  a  sense  its  origin  is  identical  with  the  wave,  v,  in  the  auricular 
venous  pulse  as  in  Figs.  44  and  45,  but  appears  earlier  in  the  cardiac  cycle 
(synchronous  with  the  carotid  pulse)  because  there  is  not  now  a  dilating 
auricle  interposed  between  the  vein  and  ventricle.  When  we  come  to  analyse 
tracings  of  the  ventricular  venous  pulse  with  a  standard  movement,  as  in 


THE  VENOUS  PULSE 


117 


Fig.  53,  we  discover  there  is  no  evidence  of  an  auricular  wave,  nor  of  a  fall 
corresponding  to  the  fall  x  in  the  auricular  venous  pulse — in  other  words, 
there  is  one  great  wave  (v)  synchronous  with  the  ventricular  systole,  and 
one  great  fall  (?/)  synchronous  with  the  ventricular  diastole.  Another  point 
to  be  noticed  is  that  the  rhythm  frequently  is  irregular,  and  that  when 
there  is  a  long  diastolic  period  there  is  a  rise  in  the  tracing  due  to  the  vein 
filling,  as  after  the  long  pauses  in  Fig.  54. 

There  are  two  conditions  which  produce  the  ventricular  form  of  the 
venous  pulse  : — 

(1)  Great  distension  and  paralysis  of  the  right  auricle.  Here  there  is 
great  engorgement  of  the  right  heart  so  that  the  auricle  becomes  embarrassed 


Fig.  54.  Simultaneous  tracings  of  the  jugular  and  radial  pulses,  showing  the  ventricular 
jugular  pulse,  i.  e.  one  large  wave,  v,  synchronous  with  and  due  to  the  ventricular  systole,  and 
one  large  fall,  y,  synchronous  with  and  due  to  the  ventricular  diastole.  The  rhythm  of  the  heart 
is  continuously  irregular.  When  there  are  long  pauses  the  tracing  of  the  jugular  gradually  rises 
before  the  next  large  wave,  on  account  of  stasis  in  the  veins.  When  the  pause  is  short  there 
is  no  sign  of  stasis,  or  only  a  slight  wave,  as  on  the  second  beat,  where  it  might  simulate  a  wave 
due  to  the  auricle,  but  the  real  cause  is  seen  to  be  stasis  in  the  veins  when  the  pause  is  longer. 

injts  action,  and  the  a  wave  in  the  jugular  pulse  diminishes  in  size  and 
disappears,  while  the  v  wave  increases  in  size  and  occupies  the  whole  period 
of  ventricular  systole.  With  recovery  and  diminution  of  the  engorgement 
the  auricular  wave  reappears.  It  is  to  be  noted  that  the  rhythm  in  these 
cases  is  always  regular.  This  manner  of  production  of  the  ventricular 
venous  pulse  is  however  very  infrequent,  far  less  common  than  what  my 
earher  observations  led  me  to  suppose,  for  the  vast  majority  of  cases  of  the 
ventricular  venous  pulse  are  due  to 

(2)  A  change  in  the  starting-point  of  the  heart's  contraction.  In  con- 
sequence of  its  great  importance  I  deal  with  the  matter  in  detail,  and  adduce 
further  proof  of  the  nature  of  the  change  in  Appendix  II.  For  the  sake  of 
brevity,  I  summarize  here  the  facts  which  show  that  the,  ventricular  venous 
pulse  is  usually  an  evidence  of  the  starting  of  the  rhythm  of  the  heart  at 
some  place  other  than  at  the  mouth  of  the  veins.  For  reasons  to  be  given  later, 
I  assume    that  this  starting-place  is  in  or  about  the  a.-v,  node  (Fig.  2), 


118  DISEASES  OF  THE  HEART 

and  hence  refer  to  this  rhythm  of  the  heart,  where  there  is  a  ventricular 
venous  pulse,  as  the  '  nodal  rhythm  '. 

The  onset  of  the  nodal  rhythm  is  characterized  by  : — 

(a)  Change  of  the  venous  and  liver  pulses  from  the  auricular  type  to  the 
ventricular. 

{b)  The  disappearance  of  all  other  evidence  of  the  auricular  systole  from 
its  normal  place  in  the  cardiac  cycle  (as  the  disappearance  of  a  presystolic 
murmur,  and  the  absence  of  an  auricular  wave  in  the  tracing  from  the 
apex  beat). 

(c)  In  many  cases  there  is  a  continued  irregularity  in  the  heart's  action. 

It  so  happened  that  my  earher  cases  of  the  ventricular  form  of  the  venous 
and  liver  pulses  were  all  secondary  to  disease  of  the  mitral  valve,  and  at  the 
post-mortem  examinations  I  found  the  right  auricle  enormously  distended 
and  the  muscle-fibres  greatly  atrophied,  so  that  I  surmised  that  the  auricle, 
like  an  over-distended  bladder,  had  become  paralysed.  This  view  seemed 
to  be  confirmed  by  the  results  of  careful  observation  of  individual  patients 
extending  over  many  years,  the  auricular  wave  never  putting  in  an  appear- 
ance at  its  normal  period  in  the  hundreds  of  tracings  I  had  taken.  This 
view  I  expressed  in  my  book  on  the  Pulse  ^^,  but  shortly  after  writing  it  a 
few  cases  came  under  my  observation  that  gave  me  grounds  for  suspecting 
that  *  auricular  paralysis  '  was  not  the  only  condition  that  gave  rise  to  the 
ventricular  form  of  the  venous  pulse. 

I  therefore  began  an  inquiry  into  all  forms  of  arrhythmia,  and  collected 
a  large  number  of  cases.  From  amongst  these  I  was  able  to  differentiate 
a  group  of  over  six  hundred  cases  in  which  the  irregularity  was  of  a  disorderly 
nature,  as  in  Figs.  53  and  54.  Over  one-half  of  these  cases  had  a  venous 
pulse,  and  in  every  case  it  was  of  the  ventricular  form.  In  more  than  fifty 
cases  the  disorderly  rhythm  had  started  while  the  patient  was  under  observa- 
tion, and  it  invariably  accompanied  the  sudden  change  of  the  jugular  pulse 
from  the  auricular  form  to  the  ventricular. 

In  a  careful  analysis  of  a  great  number  of  my  cases,  I  found  that  in  some 
there  was  only  the  large  wave,  lasting  from  the  time  of  the  opening  of  the 
aortic  valves  to  the  opening  of  the  tricuspid  valves,  as  in  Figs.  53  and  54. 
On  the  other  hand,  there  were  others  in  whom  there  could  be  seen  in  the 
jugular  veins  in  the  neck  two  movements  during  ventricular  systole — the 
first  movement  short  and  abrupt,  followed  by  a  larger  movement.  These  two 
movements  appeared  in  the  tracings  (a'  and  v  in  Figs.  55,  56,  210,  and  211). 
The  time  of  the  appearance  of  a'  was  exactly  that  of  the  carotid  in  the 
majority  of  cases  (perpendicular  hne  3  in  Fig.  55).  In  a  few  instances 
I  found  this  wave  a  little  earlier.      Thus,  in  Fig.  56  it  appears  before  the 


THE  VENOUS  PULSE 


119 


carotid  and  corresponds  with  the  beginning  of  ventricular  systole,  as  is 
shown  in  Fig,  57.  The  patient  from  whom  this  tracing  was  taken  is  described 
in  the  Appendix  II  (Case  7),  and  she  had  shown  this  form  of  jugular  pulse 


Fig.  55.  The  jugular  pulse  is  of  the  ventricular  form  and  shows  two  waves,  a'  and  v, 
during  the  period  of  ventricular  systole  (3  to  6).  The  wave  a'  appears  at  the  same  time  as  the 
carotid  pulse  (perpendicular  line  3),  and  is  due  to  the  auricle  contracting  during  the  ventri- 
cular systole.  There  is  a  notch  in  the  v  wave  (perpendicular  line  5)  corresponding  to  the  notch 
in  the  v  wave  in  Figs.  44  and  45. 

for  over  five  years.  At  the  post-mortem  examination,  the  taenia  terminalis 
of  the  auricle  was  hj^pertrophied  ;  it  can  therefore  be  inferred  that  the 
auricle  must  have  contracted.     There  Avas  never  any  sign  of  the  auricular 


Fig.  56.  Ventricular  venous  pulse.  There  are  two  waves  (a'  and  f )  in  the  jugular  puke, 
and  the  wave  a'  appears  slightly  before  the  carotid  (perpendicular  line  3),  and  is  due  to  the 
auricle  beginning  to  contract  at  the  same  time  as  the  ventricle. 

wave  before  the  carotid  pulse,  and  I  therefore  concluded  that  the  wave 
a'  in  Figs.  56  and  57  must  have  been  due  to  the  auricular  systole,  and  that 
in  these  cases  the  auricle  and  ventricle  contracted  almost  simultaneously 
(see  also  Case  12,  Appendix  II). 


120 


DISEASES  OF  THE  HEART 


Assuming  this  interpretation  to  be  correct,  it  will  be  found  that  the  wave 
a'  appears  at  the  same  time  as  the  carotid  (perpendicular  line  3  in  Fig.  55). 
As  the  ventricle  is  in  systole  before  the  aortic  valves  open,  the  ventricular 
contraction  must  have  preceded  the  contraction  of  the  auricle  which  pro- 


FiG.  57.  Tracings  of  the  ventricular  venous  pulse  and  of  the  apex  beat. 
There  are  two  waves,  a'  and  v,  in  the  venous  pulse,  and  the  wave  a'  is  seen 
to  appear  at  the  beginning  of  ventricular  systole.  The  sounds  of  the  heart 
(1  and  2)  are  represented  under  the  apex  tracing,  and  the  shading  after  2  repre- 
sents the  mitral  diastoUc  murmur.  During  the  short  pause  it  fills  up  the  whole 
period  between  the  first  and  second  sounds,  whereas  when  the  pause  is  long,  it 
stops  some  distance  before  the  first  sound. 


FiQ.  58.  Tracings  showing  the  normal  ventricular  and  auricular  movements  from  a  dog's 
heart.  The  downward  movement  represents  the  contraction.  The  perpendicular  lines,  a, 
indicate  the  beginning  of  auricular  systole,  and,  in  the  ventricular  tracing,  are  seen  to  precede 
the  ventricular  contraction.    Compare  with  Fig.  59.     (Cushny.) 

duced  the  wave  a'.  On  the  other  hand,  in  such  a  rare  instance  as  that 
shown  in  Figs.  56  and  57  the  auricle  and  ventricle  must  have  started  together. 
A  remarkable  confirmation  of  this  view  has  been  recently  obtained  by 
Cushny  ^^'  and  Lewis.  In  experimenting  on  the  dog  they  have  been  able 
to  produce  in  various  ways  an  abnormal  rhythm  of  the  heart  agreeing 


THE  VENOUS  PULSE  121 

exactly  with  the  description  given  above — that  is,  the  ventricle  started 
one-tenth  of  a  second  or  less  before  the  auricle  (see  Figs.  58  and  59),  or  the 
ventricle  and  auricle  started  simultaneously.  Lewis  has  demonstrated  the 
disappearance  of  the  auricular  systole  from  the  normal  place  in  the  cardiac 
cycle  in  cases  of  nodal  rhythm  by  means  of  electro-cardiograms  (see  Fig.  279, 
Appendix  VII). 

§  Ii6.  Conditions  giving  rise  to  a  venous  pulse To  a  great  extent 

we  are  even  at  this  day  quite  at  a  loss  to  explain  all  the  conditions  that  give 
rise  to  a  venous  pulse.  Most  people  in  good  health  show  it,  while  in  cases 
of  marked  heart  failure  it  may  be  entirely  absent.     Some  people  when  in 


VentYicle                ^'                           «•'                         ^' 

mamammim 

.1                              «''                                 ft''                                 a-' 

tTTrTTTTTTl 

8 

Fig.  59.  Tracings  of  the  movements  of  the  ventricle  and  auricle  from  a  dog's  heart, 
poisoned  by  aconitin.  The  perpendicular  lines,  a',  indicate  the  beginning  of  auricular  systole, 
and  in  the  ventricular  tracing  are  seen  to  follow  the  beginning  of  the  ventricular  contraction. 
Compare  with  Fig.  58.     (Cushny.) 

robust  health  show  no  signs  of  it,  but  if  they  become  slightly  debilitated 
the  venous  pulse  may  appear  in  the  neck.  In  some  cases  of  pernicious 
anaemia  the  venous  pulse  may  be  a  very  prominent  symptom,  in  others  it 
may  never  appear.  Some  women  during  pregnancy  develop  a  large  venous 
pulse,  others  only  develop  it  during  the  puerperium,  while  others  never 
show  the  slightest  sign  of  it.  In  irregular  action  of  the  heart  it  may  assume 
in  certain  cases,  enormous  proportions  ;  in  other  cases  there  is  not  the 
slightest  sign.  A  man  may  show  it  during  one  attack  of  heart  failure,  and 
during  another  and  more  grievous  attack  it  may  be  absent. 

I  have  endeavoured  to  find  out  the  reason  for  this  variability,  but 
though  in  some  cases  I  have  been  able  to  connect  its  appearance  and  dis- 
appearance with  definite  changes  in  the  heart,  yet  on  the  whole  the  matter 
is  one  which  still  puzzles  me. 


CHAPTER    XIV 

Enlargement  and  Pulsation  of  the  Liver 

§  117.  Reflex  or  protective  symptoms. 

118.  Signs  of  enlargement  of  the  liver. 

119.  Pulsation  of  the  liver. 

120.  Conditions  producing  enlargement  and  pulsation  of  the  liver. 

121.  Jaundice. 

122.  Differential  diagnosis. 

123.  Prognosis. 

124.  Treatment. 

The  symptoms  arising  from  enlargement  of  the  liver  due  to  heart  failure 
receive  Httle  consideration  from  clinicians,  and  are  very  frequently  over- 
looked or  misunderstood.  To  a  certain  extent,  this  is  due  to  the  fact  that 
this  enlargement  may  appear  at  such  an  advanced  stage  of  cardiac  failure 
that  the  diagnosis  and  treatment  can  be  determined  without  paying 
particular  attention  to  the  Hver  symptoms.  Graham  Steell  ^^^  includes  the 
enlargement  of  the  liver  as  one  of  the  cardinal  symptoms  of  heart  failure,  and 
Salaman^-*  has  given  a  very  suggestive  analysis  of  the  pathological  changes 
and  the  conditions  inducing  them  ;  but  clinicians  generally  have  dealt  with 
the  subject  in  a  most  perfunctory  manner.  While  it  is  true  that  the  con- 
ditions producing  these  liver  troubles  imply  an  advanced  stage  of  heart 
failure,  yet  the  recognition  of  the  symptoms  have  an  important  bearing 
on  diagnosis  and  treatment  in  many  cases.  The  symptoms  due  to  changes 
in  this  organ  are  not  always  easy  to  understand,  but  that  is  no  reason  for 
ignoring  them. 

§  117.  Reflex  or  protective  symptoms Usually  in  the  early  stages 

of  liver  enlargement  we  find  evidences  of  the  intervention  of  the  protective 
mechanism  (see  Chapter  VI).  While  the  Hver  may  be  only  one  or  two 
inches  below  the  ribs,  the  muscle  wall  of  the  upper  part  of  the  right  half  of 
the  abdomen  becomes  hard  and  tender.  This  tenderness  is  invariably  put 
down  to  the  hver  itself,  and  the  manner  in  which  this  *  tenderness  '  is 
usually  demonstrated  is  by  eliciting  pain  on  pressing  the  finger  into  the 
patient's  abdomen.  But  if  the  extent  of  the  hyperalgesia  and  the  size  of 
the  liver  be  mapped  out,  it  will  be  found  that  the  former  is  far  more 
extensive  than  the  latter,  and  sometimes  extends  round  to  and  affects  the 


ENLARGEMENT  AND  PULSATION  OF  THE  LIVER  123 

erector-spinae  muscles.  In  some  cases  the  skin  and  subcutaneous  tissue 
also  become  tender,  but  they  rarely  become  so  sensitive  as  the  muscles. 
Sometimes  there  seems  an  increased  tenderness  where  the  liver  is  reached, 
but  this  wiU  be  found  to  be  due  to  the  more  effective  compression  of  the 
muscle  between  the  finger  and  the  liver.  There  are  many  other  ways 
by  which  the  resourceful  observer  can  demonstrate  the  tissue  in  which  the 
tenderness  is  present. 

The  consequence  of  this  muscular  hyperalgesia  is  manifested  in  various 
ways.  If  the  patient  is  going  about  he  may  suffer  severe  pain  across  the 
upper  part  of  the  abdomen  or  in  the  back,  this  probably  being  due  either 
to  increased  engorgement  of  the  liver  or  to  the  increase  of  the  pain  in  con- 
sequence of  the  exercise  of  the  hyperalgesic  muscles.  This  tenderness  and 
rigidity  of  the  abdominal  muscles  interferes  with  the  respiration  of  the 
patient.  He  cannot  breathe  deeply,  and  attempts  to  do  so  are  painful, 
hence  there  results  rapid  and  shallow  breathing,  with  further  embarrassment 
of  the  right  heart  and  a  tendency  to  pulmonary  stasis. 

With  long-continued  persistence  of  the  enlargement,  all  the  sensory 
phenomena  disappear,  the  abdominal  wall  becomes  lax,  and  sometimes 
the  edge  of  the  Uver  can  be  grasped. 

§  Ii8.  Signs  of  enlargement  of  the  liver — It  is  not  always  easy 
to  make  out  the  enlargement  of  this  organ.  The  contracted  muscles  often 
prevent  the  palpation,  and  even  percussion  helps  but  little.  Ascitic  and 
gaseous  distension  add  further  to  the  difficulty.  But  with  care  and  gentle- 
ness in  palpation  one  may  overcome  the  resisting  muscles.  Even  when  the 
edge  of  the  liver  cannot  be  made  out,  the  peculiar  sense  of  resistance  conveyed 
to  the  exploring  hand  may  reveal  the  enlarged  liver.  Other  methods  may 
be  adopted,  such  as  pushing  the  liver  forward  with  one  hand  while  the  other 
explores  the  front.  When  the  muscles  relax  and  the  hyperalgesia  disappears, 
there  is  no  difficulty  in  finding  out  the  enlarged  Hver,  except  when  there  is 
great  distension  of  the  abdomen. 

§  119.  Pulsation  of  the  liver — When  the  liver  is  enlarged  from  heart 
failure  it  not  infrequently  pulsates.  If  the  abdominal  muscles  are  lax, 
there  is  no  difficulty  in  recognizing  this.  If  one  hand  presses  on  the  liver 
behind  and  the  other  is  laid  on  it  in  front,  the  latter  is  heaved  up  and  down 
with  the  pulse.  Even  where  there  is  a  considerable  amount  of  muscular 
contraction,  exploring  the  edge  of  the  liver  with  the  liver  receiver  will 
often  reveal  the  pulsation  (§  71). 

There  are  two  forms  of  liver  pulse,  corresponding  to  the  two  forms  of 
venous  pulse — an  auricular.  Fig.  60,  and  a  ventricular,  Fig.  61,  the  latter  being 
an  evidence  of  the  nodal  rhythm.     When  a  liver  pulse  and  a  jugular  pulse 


124 


DISEASES  OF  THE  HEART 


are  both  present  in  the  same  individual,  they  are  always  of  the  same  form. 
In  Fig.  62  a  tracing  of  an  am-icular  jugular  pulse  is  taken  simultaneously 
with  a  tracing  of  the  auricular  liver  pulse.     In  Fig.  63,  the  tracing  of  the 


LiveT 

T  I        f 

a 

a 

\ 

V 

arts 

\ 

1 

1^ 

Ij 

Fig.  60.     The  liver  pulse  is  of  the  auricular  form  and  shows  a  well-marked 

auricular  wave,  a. 

ventricular  jugular  pulse  is  seen  to  be  identical  with  the  liver  pulse  in 
Fig.  61,  both  tracings  being  from  the  same  patient. 

§  120.  Conditions  producing  enlargement  and  pulsation  of  the  liver. 
— I  have  already  remarked  on  the  variety  of  conditions  producing  the  jugular 


Fig.  61.     The  liver  pulse  is  of  the  ventricular  form,  showing  no  auricular  wave. 

pulse,  and  there  is  a  Mke  difficulty  in  understanding  the  conditions  which 
give  rise  to  liver  enlargement.  Cases  otherwise  identical  in  their  symptoms, 
and'  suffering  from  heart  failure  due  to  the  same  cause,  may,  diifer  in  this 


Jit.l7-lt..Ju(/. 

rt  „ 

^  n           '^n 

:           ■                                   1         i..l 

a 

a?           as                      '                         j  - 

'     1   1 

!   .  -^ 

Liver                         !       1 

a 

a 

a         a. 

AtAa 

I\jAAM 

A       A 

X 

X 

Fig.  62.  Simultaneous  tracings  of  the  jugular  and  liver  pulses,  showing 
the  correspondence  between  the  waves  a  and  v,  and  the  absence  of  the  carotid 
wave  c  from  the  liver  pulse. 

particular,  some  showing  enlargement  of  the  hver  and  others  faihng  to  do 
so.  Similarly  it  is  not  always  quite  clear  why  some  pulsate  while  others 
do  not.     To  a  certain  extent,  I  think  this  is  due  to  the  condition  of  the  right 


ENLARGEMENT  AND  PULSATION  OF  THE  LIVER  125 

auricle.  It  takes  some  force  to  distend  the  liver,  and  normally  the  right 
am*icle  has  not  sufficient  strength,  so  that  as  long  as  the  right  auricle  contracts 
and  dilates  in  its  normal  place  in  the  cardiac  cycle  it  prevents  the  ventricle 
exercising  its  force  on  the  liver.  When,  however,  the  ventricle  starts  the 
rhythm,  it  drives  the  blood  through  the  incompetent  tricuspid  orifice  with 
such  force  that  the  liver  pulsates.  It  is  in  the  cases  of  nodal  rhythm  that 
we  most  frequently  find  the  liver  pulsating.  When  the  nodal  rhythm  is 
transient  the  liver  may  quickly  enlarge  and  pulsate,  and  with  cessation  of 
the  attack  as  quickly  subside  and  cease  to  beat — the  liver  pulse  being  of  the 
ventricular  form  (Fig.  207). 

Reasoning  that  it  requires  some  force  greater  than  the  normal  strength 
of  the  right  auricle  to  produce  pulsation  of  the  liver,  I  at  first  drew  the 


Fig.  63.  Simultaneous  tracings  of  the  jugular  and  radial  pulses.  The  jugular  pulse  is  of 
the  ventricular  form  and  is  identical  with  the  liver  pulse  in  Fig.  61,  both  being  taken  from  the 
same  patient. 

conclusion  that  an  auricular  liver  pulse  indicates  hypertrophy  of  the  right 
auricle,  and  as  this  occurs  most  characteristically  in  cases  of  tricuspid 
stenosis,  I  regarded  the  auricular  liver  pulse  as  diagnostic  of  tricuspid 
stenosis.  All  the  cases  that  had  shown  this  auricular  liver  pulse  during  life, 
whose  hearts  I  examined  'post  mortem,  showed  tricuspid  stenosis.  But  I  have 
now  had  a  number  of  cases  showing  this  form  of  liver  pulse,  in  which  I  doubt 
if  I  am  justified  in  assuming  tricuspid  stenosis.  Volhard^'^  describes  the 
auricular  liver  pulse  in  pericardial  effusion,  and  Wenckebach  ^^^  in  a  case  of 
adherent  pericardium. 

§  121.  Jaundice. — Jaundice  is  a  frequent  accompaniment  of  enlarge- 
ment of  the  liver  ;  though  of  itself  of  little  importance,  it  should  be  kept 
in  mind  that  a  slight  jaundice  may  be  misleading.  Many  patients  with 
.advanced  heart  failure  and  with  the  nodal  rhythm  get  rapidly  thinner. 
In  these  the  liver  is  sometimes  greatly  enlarged,  so  that  the  wasting  of  the 
patient,  the  enlargement  of  the  liver,  and  the  jaundiced  tint,  present  the 
features  of  malignant  disease  of  the  liver,  and  I  have  seen  cases  presenting 
these  symptoms  thus  wrongly  diagnosed. 


126 


DISEASES  OF  THE  HEART 


§  122.  Differential  diagnosis — Many  writers  refer  to  an  '  arterial 
pulsation  '  of  the  liver,  and  I  have  often  wondered  what  they  mean,  par- 
ticularly as  no  details  are  ever  given.  I  have  never  found  any  condition 
that  could  come  under  this  heading,  and  I  suspect  that  some  observers 
have  mistaken  the  movement  of  the  liver,  when  it  is  pulled  up  and  down 
with  the  systole  and  diastole  of  the  ventricle,  for  a  pulsation,  particularly 
as  it  is  sometimes  mentioned  in  connexion  with  aortic  regurgitation. 
Wherever  there  is  much  cardiac  enlargement,  movement  of  the  liver  is 
produced.  Even  in  patients  with  normal  hearts  but  with  lax  abdominal 
wall,  this  up-and-down  movement  can  be  recognized.  It  has  already  been 
referred  to  in  §  81.  Here  I  need  only  point  out  that  the  conditions  in 
which  it  occurs  are  generally  very  different  from  that  of  the  heart  failure 
in  which  the  true  liver  pulsation  occurs.      A  tracing  of  this  movement 


Fig.  64.    Tracings  from  the  abdominal  aorta  and  the  liver.    The  liver  pulse  is  of  the 

auricular  type. 


sets  the  matter  at  rest,  as  the  fall  due  to  the  ventricular  systole  does  not 
begin  until  the  opening  of  the  aortic  valves  and  the  expulsion  of  blood  from 
the  chest,  which  is  practically  synchronous  with  the  carotid  pulse.  In  the 
ventricular  form  of  liver  pulse,  on  the  other  hand,  there  is  a  rise  during 
ventricular  systole.  A  tracing  of  the  liver  movement  can  be  distinguished 
from  the  auricular  liver  pulse  in  that  the  fall  in  the  latter  case  precedes  the 
carotid  pulse. 

There  is  generally  little  difficulty  in  distinguishing  the  pulsation  of  the 
abdominal  aorta  from  that  of  the  liver  pulse.  In  cases  where  the  ventri- 
cular liver  pulse  is  present,  it  is  very  rarely  that  the  abdominal  aorta  can 
be  felt,  and  the  characters  of  the  tracings  are  not  likely  to  be  confused. 
The  auricular  form  of  liver  pulse  is  still  more  distinct  in  character  from  that 
of  the  abdominal  aorta,  as  shown  in  Fig.  64, 

§  123.  Prognosis. — Liver  enlargement  and  pulsation  from  cardiac 
disease  indicate  a  very  advanced  stage  of  heart  failure.  In  cases  where  the 
heart  failure  is  secondary  to  a  rheumatic  affection  of  the  heart  with  mitral 


ENLARGEMENT  AND  PULSATION  OF  THE  LIVER 


127 


disease,  it  may  only  appear  during  the  attacks  of  heart  failure  to  which 
the  patients  are  liable.  The  enlargement  subsides  with  improvement,  and 
if  the  heart's  restoration  be  good  the  patient  may  have  no  signs  of  the  liver 
enlargement  for    many   years.      Some   patients    with    the   nodal   rhythm 


Fig.  65.  Simultaneous  tracings  of  the  apex  beat 
and  of  the  liver  pulse.  The  liver  edge  was  below  the 
level  of  the  umbiUcus,  and  the  pulsation  of  great  size. 

secondary  to  rheumatic  affection  of  the  heart  may  for  years  have  a  big 
pulsating  Uver  (Fig.  65),  in  others  the  enlargement  appears  during  temporary 
heart  failure.  In  some  of  these  the  exhibition  of  digitalis  may  cause  the 
subsidence  of  the  liver  in  a  couple  of  days.    Fig.  66  was  taken  from  the  liver 


Fig.  66.     Tracings  of  the  liver  and  radial  pulses  during  a  period  of  extreme  heart 

failure  (nodal  rhythm). 

of  a  man  which  was  pulsating  as  low  as  his  umbilicus.  In  a  couple  of  days 
all  signs  of  the  liver  below  the  ribs  had  gone.  The  enlarged  liver  coming 
on  in  paroxysmal  tachycardia,  i.e.  transient  nodal  rhythm,  is  a  very  serious 
symptom,  as  it  indicates  marked  dilatation  of  the  heart.  Also  in  the  heart 
failure  due  to  cardio-sclerosis  with  the  permanent  nodal  rhythm,  it  is  a  very 


128  DISEASES  OF  THE  HEART 

grave  symptom,  as  the  heart  failure  is  due  to  extensive  degeneration  of  the 
cardiac  muscle,  and  therefore  does  not  respond  to  the  influence  of  rest 
and  digitalis.  Enlargement  of  the  liver  in  muscle  failure  due  to  chronic 
alcoholism  is  a  bad  sign. 

§  124.  Treatment. — Though  no  treatment  is  directed  specially  to  the 
liver  enlargement,  the  effect  of  the  rigid  tender  muscles  in  embarrassing 
the  respiration  should  be  borne  in  mind,  and  suitable  attempts  made  to  put 
the  patient  in  a  comfortable  position  so  that  he  can  breathe  more  easily, 
and  the  pain  due  to  the  enlarged  liver  should  caU  for  the  cessation  of  all 
exertion  that  induces  it.  A  smart  mercurial  purge  may  sometimes  afford 
considerable  relief. 


CHAPTER  XV 

Inceeased  Frequency  of  the  Heart's  Action 

§  125.  The  normal  rate. 

126.  Classification. 

127.  Cases  which  respond  to  a  call  upon  the  heart's  energy  by  increased  frequency. 

128.  Cases  in  which  the  heart's  rate  is  continuously  increased. 

129.  Cases  in  which  the  increased  frequency  of  the  heart  occurs  in  irregular  paroxysmal 

attacks  (palpitation). 

130.  The  cause  of  increased  frequency  of  the  heart's  action. 

131.  Prognosis. 

§  125.  The  normal  rate — The  rate  of  the  heart  varies  very  consider- 
ably according  to  age,  sex,  and  individual  peculiarities.  At  birth,  the  rate 
is  usually  from  130  to  140  per  minute.  With  advancing  years  the  heart 
slows  down  gradually  :  between  nine  and  ten  the  average  is  about  ninety  ; 
at  twenty,  about  seventy-four  ;  at  thirty,  from  sixty-six  to  seventy-six  : 
it  remains  at  about  this  latter  rate  until  over  fifty,  when  it  gradually  begins 
to  increase  in  frequency.  At  all  ages  very  considerable  variations  may  be 
met  with. 

The  heart's  rate  is  greatly  increased  by  exertion,  even  in  those  who  are 
in  good  training.  Deane  found  the  pulse-rate  over  200  per  minute  in 
a  professional  dancer,  at  the  end  of  a  dance.  It  quickly  subsided  to  the 
normal  rate.  According  to  Pembrey  and  Todd  the  increase  in  rate  is 
somewhat  greater  in  the  trained  than  in  the  untrained,  but  the  decrease 
in  the  rate  to  normal  is  more  rapid  in  the  trained  man. 

§  126.  Classification — In  considering  the  conditions  that  give  rise 
to  increased  frequency  of  the  heart's  action,  we  are  confronted  with  such 
a  great  number  that  it  is  impossible  to  deal  with  them  all.  What  I  propose 
to  deal  with  here  is  the  abnormal  increase  of  pulse-rate,  and  certain  con- 
ditions other  than  febrile  which  induce  the  rapidity  of  the  pulse.  These  may 
fittingly  be  discussed  in  three  groups  :  (1)  Those  cases  in  which  the  heart 
responds  to  a  call  upon  its  energy  by  increased  frequency  ;  (2)  those  cases  in 
which  the  heart-rate  is  continuously  increased  ;  (3)  those  cases  in  which  the 
periods  of  increased  rapidity  take  place  in  irregular  paroxysmal  attacks. 

§  127.  Cases  which  respond  to  a  call  upon  the  heart's  energy  by 
increased  frequency. — The  cases  in  the  first  of  these  groups,  those  in 

MACKENZIE  fr 


130  DISEASES  OF  THE  HEART 

which  the  heart  responds  to  an  increased  call  upon  its  energy  by  increased 
frequency,  show  in  reality  but  an  exaggerated  form  of  the  normal  condition. 
When  we  find  that  a  patient  is  seized  with  palpitation  or  rapid  heart  action 
after  mounting  a  few  steps,  we  recognize  as  abnormal  that  which  would  have 
been  regarded  as  normal  in  an  individual  who  had  run  half  a  mile  at  the 
top  of  his  speed.  In  other  words,  this  increased  rate  is  an  evidence  that  the 
field  of  the  heart's  response  to  effort  is  greatly  reduced.  A  further  deduction 
can  be  made  from  observing  these  patients,  viz.  that  exhaustion  of  the 
reserve  force  heightens  the  excitability  of  the  whole  heart,  for  not  only 
is  the  rate  increased,  but  the  contraction  sweeps  through  the  heart  with 
greater  rapidity  and  the  systoles  of  the  chambers  are  of  shorter  duration. 
The  increased  frequency  should  always  lead  one  to  seek  the  cause  from 
which  it  arises.  The  conditions  underlying  it  are  too  numerous  to  mention, 
but  they  all  in  the  end  point  to  enfeeblement  of  the  muscle  of  the  heart. 
In  all  exhausting  diseases,  and  after  convalescence  from  such  a  w^asting  sick- 
ness as  typhoid  fever,  the  heart's  rate  can  be  greatly  increased  by  even  very 
moderate  exertion.  In  the  various  anaemias  (chlorosis,  pernicious  anaemia, 
maUgnant  cachexia)  the  rapid  heart  action  is  very  often  the  symptom  to 
which  the  patient's  attention  is  first  called.  In  organic  affections  of  the 
heart,  as  in  the  various  forms  of  myocarditis,  in  fatty  degeneration  of  the 
myocardium,  and  in  valvular  disease  when  there  is  only  a  small  amount  of 
reserve  force  in  the  muscle,  increased  frequency  of  the  pulse  on  exertion  is 
extremely  common.  Many  of  the  patients  whose  ailments  are  included  in 
the  foregoing  groups,  when  at  rest,  have  a  pulse  beating  about  or  not  much 
above  the  normal  rate.  The  heart  then  seems  to  be  capable  of  sustaining 
the  demands  of  the  circulation,  but  seems  to  be  working  near  the  top  of 
its  reserve  energy.  On  exertion  this  reserve  energy  is  speedily  exhausted, 
and  in  order  to  make  up  for  its  inability  to  respond  to  the  demand  of  the 
tissues  for  more  blood  by  giving  stronger  ventricular  contractions,  it  responds 
by  giving  a  greater  number  of  feebler  and  less  complete  contractions. 

In  addition  to  the  increased  rate  there  is  usually  hurried  and  laboured 
respiration,  and  this  too  occurs  whether  a  strong  heart  is  overstrained  by 
a  great  effort,  or  a  weak  heart  by  a  slight  effort.  Not  infrequently  in  elderly 
people,  before  the  interference  with  respiration  can  arise,  the  patient  in 
making  an  effort  is  stopped  by  a  feeling  of  weight  or  oppression  within  the 
chest,  or  even  by  pain  striking  across  the  chest,  sometimes  severe,  sometimes 
slight,  but  in  all  cases  imperiously  demanding  a  cessation  of  the  effort. 

It  is  as  impossible  to  indicate  with  any  approach  to  accuracy  when  a  pulse- 
rate  is  abnormal  on  moderate  exertion  as  it  is  to  indicate  what  the  pulse- 
rate  should  be  in  health  under  similar  circumstances.     The  increase  is  often 


INCREASED  FREQUENCY  OF  THE  HEART'S  ACTION       131 

so  marked  that  its  recognition  is  beyond  dispute.  Thus,  in  making  a  patient 
sit  up  or  turn  over  in  bed,  a  rise  of  five  to  ten  beats  a  minute  may  not  be 
worthy  of  much  attention,  but  if  the  increase  is  fifteen  to  thirty  beats  then 
there  is  distinct  evidence  that  we  have  to  do  with  some  condition  that  has 
exhausted  the  heart's  reserve  power.  This  increase  of  the  pulse-rate  beyond 
the  normal  on  moderate  exertion  does  not  give  any  clue  to  the  nature  of  the 
condition  that  has  reduced  the  heart's  reserve  power.  As  already  indicated, 
these  conditions  are  so  numerous  that  an  examination  for  other  symptoms 
must  be  undertaken  to  discover  them. 

§  128.  Cases  in  which  the  heart's  rate  is  continuously  increased. 
{a)  Valvular  disease. — The  second  division,  in  which  the  heart  main- 
tains a  frequency  beyond  what  we  recognize  as  within  the  limits  of  health, 
also  includes  a  great  variety  of  heart  conditions.  We  have  among  these 
the  series  of  valvular  diseases  of  the  heart,  with  the  muscle  exhausted, 
it  may  be  from  struggling  against  the  obstruction  caused  by  the  valve  lesion, 
or  with  the  muscle  itself  degenerated.  Not  only  do  such  hearts  respond 
to  effort  with  marked  increase  in  frequency,  but  even  during  rest  the  heart 
may  beat  with  abnormal  rapidity,  regularly  or  irregularly.  This  forms 
a  very  important  factor  in  arriving  at  an  estimate  of  the  strength  and 
condition  of  the  organ.  The  other  symptoms  of  heart  failure  present  will 
help  in  indicating  the  stage  at  which  the  patient  has  arrived. 

(6)  Affections  of  the  myocardium. — Apart  from  patients  with  mani- 
fest valvular  disease  of  the  heart,  there  are  many  whose  pulse  is  rapid, 
and  in  whom  no  disease  of  the  heart  can  be  detected  by  physical  signs. 
The  chest- wall  may  be  thick  and  fat,  or  the  lungs  so  voluminous  that  the 
actual  size  of  the  organ  cannot  be  satisfactorily  defined.  The  sounds, 
though  free  from  murmur,  may  be  so  slightly  modified  that  no  certain  infer- 
ences can  be  drawn  from  them.  Yet  that  serious  mischief  is  present  is 
but  too  often  demonstrated  by  watching  the  after-history  of  these  cases. 
If  we  exclude  for  the  present  the  consideration  of  certain  neurotic  conditions, 
the  cause  of  the  quickening  in  all  cases  is  really  associated  with  a  want  of 
strength  in  the  muscular  wall.  In  valvular  disease  this  is  usually  spoken 
of  as  failure  of  compensation.  In  degeneration  of  the  wall,  fatty  or  fibrous, 
the  weakening  of  the  wall  is  directly  due  to  this  degeneration.  In  the 
great  series  of  hearts  overstrained  from  excessive  exertion,  the  weakness 
of  the  wall  is  the  principal  cause  of  the  whole  train  of  symptoms  associated 
with  the  failure  of  the  heart.  In  arriving,  therefore,  at  an  estimate  of  the 
value  of  the  pulse  quickening,  a  consideration  of  the  other  symptoms  present 
will  be  necessary  to  recognize  what  is  the  cause  of  the  increased  pulse-rate 
in  each  special  case.     The  circumstances,  age,  and  condition  of  the  patient, 

k2 


132  DISEASES  OF  THE  HEART 

will  help  much  in  recognizing  the  rapid  pulse  due  to  actual  degeneration  of 
the  heart-wall.  But  there  is  a  series  of  cases  in  which  it  is  difficult  to  account 
for  the  rapid  pulse,  especially  when  it  occurs  in  the  apparently  strong  in  the 
prime  of  life.  In  these  cases  there  is  generally  a  history  of  hard  work  or 
periods  of  excessive  muscular  exertion.  Sometimes  the  condition  receives 
a  special  name,  as  '  the  soldier's  heart  '.  Medical  men  whose  practice  lies 
amongst  workpeople  subjected  to  such  muscular  exertion  are  familiar  with 
a  similar  condition.  The  heart  overstrain  is  most  evident  amongst  those 
with  a  tendency  to  obesity  and  who  indulge  rather  freely  in  alcohol. 
The  symptoms  are  mainly  a  quickened  pulse  and  shortness  of  breath  on 
exertion.  Examination  of  the  chest  is  often  fruitless,  the  chest  being  large 
and  deep,  and  the  lungs  often  voluminous.  Much  improvement  results 
from  care  and  rest,  and  appropriate  treatment. 

(c)  Pregnancy. — It  may  be  noted  that  these  symptoms  are  often 
present  in  pregnant  women,  but  there  the  cause  is  but  temporary,  and  a 
certain  amount  of  recovery  follows  delivery.  But  in  my  experience  there 
is  often  left  a  certain  amount  of  cardiac  weakness,  shown  by  a  distinct 
limitation  of  the  field  of  cardiac  response. 

{d)  Alcohol. — In  all  obscure  cases  of  rapid  heart  action,  the  question 
of  over-indulgence  in  alcohol  should  be  carefully  inquired  into.  The  patients 
often  try  to  hide  their  habits  in  this  respect,  but  the  physician  can  generally 
find  a  clue  in  the  manner  of  the  individual,  his  facial  aspect,  tremulous 
muscles  (especially  the  tongue),  want  of  appetite  or  nausea  in  the  morning, 
and  that  tout-ensemble  which  leads  the  experienced  physician  to  suspect 
the  secret  alcoholic.  Accompanying  the  rapid  pulse  and  other  phenomena 
there  are  often  a  sinking  sensation  in  the  epigastrium  and  sense  of  exhaustion 
on  exertion,  and  breathlessness.  The  heart  may  be  only  slightly  enlarged, 
or  there  may  be  great  dilatation,  usually  accompanied  by  enlargement  of 
the  liver  and  tenderness  of  the  tissues  covering  it.  With  abstinence  from 
alcohol  these  cases  in  the  early  stages  quickly  recover,  but  with  continuance 
of  the  habit  all  the  characters  of  severe  heart  failure  supervene. 

(e)  Neurotic  cases. — There  is  a  group  of  people  who  exhibit  a  rapid 
pulse  in  whom  no  heart  lesion  can  be  detected,  and  whose  future  history 
demonstrates  that  no  serious  cardiac  lesion  existed.  These  people  exhibit 
other  symptoms  more  prominently  associated  with  the  nervous  system, 
and  are  described  in  Chapter  VIII. 

(/)  Exhausting  diseases. — It  is  always  well  to  bear  in  mind  that  a 
persistent  quick  pulse  may  be  the  earliest  symptom  of  an  attack  of  tuber- 
culosis or  of  the  onset  of  malignant  disease.  A  patient  may  complain  for 
months  of  weakness,  with  an  absence  of  the  sense  of  well-being,  with  no  actual 


INCREASED  FREQUENCY  OF  THE  HEART'S  ACTION       133 

suffering.  After  a  time  the  development  of  other  symptoms  demonstrates 
the  cause  of  the  abnormal  pulse-rate.  In  the  young,  particularly,  persistent 
high  frequency  of  the  heart's  action  in  the  absence  of  any  demonstrable 
heart  lesion  should  always  awaken  the  suspicion  of  a  latent  tubercular 
affection.  I  have  watched  such  cases  for  months,  and  puzzled  over  the 
cause  of  the  rapid  heart-action,  until  the  true  nature  of  the  complaint  was 
revealed  by  some  definite  sign  such  as  the  pointing  of  a  psoas  abscess  or  a 
pulmonary  haemorrhage.  In  most  exhausting  diseases  (malignant  diseases, 
pernicious  anaemia,  tuberculosis)  the  pulse-rate  is  continuously  quickened. 
The  frequent  heart-action  may  usually  be  taken  to  indicate  a  severe  infection 
and  a  serious  condition. 


Fig.  67.    From  a  female  aged  forty,  suffering  from  exophthalmic  goitre.    Rate  120.   ' 


Fig.  68.  From  a  female  aged  twenty-two,  suffering  from  exophthalmic  goitre.    Rate  120. 

(g)  Exophthalmic  goitre. — The  essential  features  arising  from  the  circu- 
lation in  many  cases  of  exophthalmic  goitre,  it  seems  to  me,  are  the 
abnormal  and  persistent  dilatation  of  the  arterioles,  and  a  heart  acting 
with  a  force  relatively  great  to  the  resistance  opposed.  These  are  indicated 
by  the  rapid  and  forcible  pulse-wave  felt  by  the  finger,  and  the  visible 
pulsation  of  the  superficial  arteries  and  the  carotid.  The  corresponding 
sphygmographic  features  are  a  high  upstroke  and  rapid  fall,  so  that  the 
dicrotic  notch  is  near  the  base  line  (Figs.  67  and  68).  The  rate  of  the 
pulse  may  be  greatly  increased,  up  to  140-160  per  minute.  The  same 
factors,  the  unusually  forcible  injection  of  the  blood  into  the  arteries  of 
low  blood-pressure,  are  present  in  aortic  regurgitation.  Though  the  beating 
of  the  carotid  is  due  to  similar  causes  in  the  two  cases,  the  low  arterial 
pressure  at  the  end  of  diastole  is  different.  In  exophthalmic  goitre  the 
dilatation  of  the  arterioles  and  capillaries  is  the  sole  cause,  whereas  in 
aortic  regurgitation  there  is  in  addition  the  backward  flow  into  the  ventricle 
through  the  incompetent  valves.  The  condition  of  the  circulation  in 
exophthalmic  goitre  is  also  comparable  to  that  in  some  forms  of  sthenic 
fever,  where  the  heart  beats  forcibly  and  the  arteries  are  relaxed. 

Another  evidence  of  the  relaxation  of  the  arterioles  is  to  be  found  in  the 


134  DISEASES  OF  THE  HEART 

subjective  sensation  of  warmth  felt  by  some  sufferers  from  exophthalmic 
goitre.  They  rarely  complain  of  cold  in  winter,  however  lightly  clad  they 
are,  and  this  is  not  infrequently  the  cause  of  matrimonial  disputes,  for  while 
the  ailing  wife  feels  warm  in  bed  during  winter  with  few  blankets,  the  healthy 
husband  feels  the  cold  keenly.  This  feehng  of  warmth  has  supplied  me  with 
the  indications  for  the  only  treatment  of  this  class  of  case  that  I  have  foimd 
both  grateful  and  beneficial  to  the  patient,  namely,  the  periodic  stimulation 
of  the  vaso-motor  nerves  by  cold  baths.  Whenever  the  feehng  of  warmth 
has  been  present  I  have  found  these  baths  do  good,  and  when  there  is 
nervousness  and  muscular  tremor  the  administration  of  the  bromide  of 
ammonium  has  been  of  great  service. 

§  129.  Cases  in  which  the  increased  frequency  of  the  heart 
occurs  in  irregular  paroxysmal  attacks — This  class  includes  cases  of 
'  palpitation  '  and  '  paroxysmal  tachycardia  '.  There  are  quite  a  number  of 
different  conditions  included  under  these  terms,  and  no  clear  idea  is  usually 
given  of  what  is  meant.  A  very  useful  and  practical  division  may  be  based 
on  the  manner  in  which  the  heart's  contraction  starts.  In  the  vast  majority 
of  cases  of  transient  rapid  heart-action,  the  heart's  action  is  perfectly  normal  ; 
the  rapid  action  of  this  class  will  be  spoken  of  here  as  '  attacks  of  palpitation  '. 
In  another  class  of  patient  the  heart's  contraction  does  not  start  at  the 
normal  place  ;  to  this  latter  class  the  term  '  paroxysmal  tachycardia  '  is 
limited,  and  the  cases  are  described  in  the  sections  on  '  nodal  rhythm  ' 
(p.  309)  and  auricular  tachycardia  (p.  334). 

The  rate  in  the  first  class  rarely  exceeds  170  beats  per  minute,  and  the 
rhythm  is  regular  except  for  the  presence  of  an  occasional  extra-systole  ;  in 
the  latter  class  the  rate  may  at  first  exceed  200  beats  per  minute,  and  the 
rhythm  is  frequently  irregular.  (Concerning  the  records  of  extreme  fre- 
quency sometimes  quoted,  I  may  say  I  have  never  met  with  cases  approach- 
ing 300  per  minute,  nor  have  I  come  across  a  single  instance  of  a  published 
tracing  recording  such  a  speed.  They  may  be  pubHshed,  but  I  have  not 
seen  them.  I  have  a  suspicion  of  any  estimate  made  of  a  pulse-rate  over 
200  unless  graphically  recorded,  because  I  doubt  if  the  human  mind  is 
capable  of  accurately  distinguishing  between  events  occurring  at  a  speed 
over  200  per  minute,  and  I  doubt  if  any  one  could  articulate  or  mentally 
distinguish  the  individual  numbers  at  a  rate  of  300  per  minute.) 

In  the  following  paragraph  I  describe  under  '  palpitation  '  the  more 
common  forms  of  temporary  rapid  action  of  the  heart. 

Palpitation. — This  may  occur  in  people  suffering  from  a  great  variety 
of  complaints.  The  patient  is  usually  conscious  of  the  change  in  the  heart's 
action,  feeling  the  rapid  beats  and  sometimes  describing  them  as  gentle, 


INCREASED  FREQUENCY  OF  THE  HEART'S  ACTION        135 

sometimes  as  hard  and  hammering.  These  latter  sensations  may  occur 
with  httle  or  no  increase  in  frequency.  In  cases  of  valvular  disease  with 
limited  reserve  force,  slight  physical  effort  or  mental  excitement  may 
readily  induce  an  attack.  Even  in  the  healthy,  certain  mental  states  may 
induce  an  attack,  while  when  the  system  is  weakened  from  disease  the 
liabiUty  to  attack  is  much  increased.  It  is  in  certain  neurotic  subjects, 
particularly  females,  that  one  sees  the  complaint  attain  its  most  distinctive 
features.  There  may  be  no  organic  affection  of  the  heart,  and  though 
frequent  attacks  may  ultimately  induce  exhaustion  of  the  reserve  force. 


Fig.  69.     During  an  attack  of  palpitation.    Kate  105. 

yet,  as  a  rule,  they  do  not  appreciably  shorten  life.  Anything  that  startles 
the  patient,  whether  a  sudden  noise  or  mental  perturbation  when  awake, 
or  uncomfortable  dreams  when  asleep,  readily  induces  an  attack.  But 
it  may  supervene  from  more  obscure  causes,  evidently  caused  by  reflexes 
from  organs  more  or  less  remote  (stomach,  uterus),  or  from  undiscernible 
sources.  When  a  severe  attack  comes  on  the  patient  may  become  painfully 
aware  of  the  violent  action  of  the  heart.  She  prefers  to  sit  upright,  draws 
deep  inspirations,  and  moves  uneasily  from  side  to  side,  with  the  hand 
pressed  over  the  heart.  It  is  accompanied  by  sensations  of  a  distressing 
nature,  such  as  a  sense  of  suffocation,  and  a  fear  of  impending  dissolution. 
When  it  subsides  it  leaves  the  patient  exhausted. 


Fig.  70.     Tracing  of  the  normal  pulse  of  the  patient  from  which  Fig.  69  was  obtained. 

Rate  64. 

During  the  attack  the  pulse  is  usually  increased  in  frequency.  The  artery 
may  be  of  fair  size  ;  sometimes,  however,  it  is  very  small.  The  impact  of 
the  pulse-wave  on  the  finger  is  sudden  and  sharp  and  of  extremely  brief 
duration.  The  tracing  Fig.  69,  taken  during  an  attack  of  palpitation, 
shows  a  high  upstroke  with  a  great  fall,  so  that  the  arterial  pressure  at 
the  bottom  of  the  dicrotic  notch  is  nearly  as  low  as  at  the  end  of  the 
diastohc  period — an  evidence  that  in  addition  to  the  excited  heart  there 
is  great  relaxation  of  the  arterial  wall.  Fig.  70  is  from  the  same  patient 
when  the  heart  was  acting  quietly. 


136 


DISEASES  OF  THE  HEART 


We  occasionally  meet  with  patients  in  whom  the  pulse  is  extremely 
rapid  for  a  period,  sometimes  for  a  few  minutes,  sometimes  for  a  few 
hours,  with  no  other  sensation  than  that  of  exhaustion,  the  attack  quietly 
subsiding  (Fig.  71).  The  causes  are  so  obscure  that  it  would  be  mere 
guesswork,  in  the  majority  of  cases,  to  attribute  it  to  any  one  cause. 

§  130.  The  cause  of  increased  frequency  of  the  heart's  action. — 
Apart  from  cases  due  to  nerve  excitation,  and  the  nodal  rhythm,  it  is 
extremely  difficult  to  account  properly  for  this  abnormal  quickening.  All  the 
parts  of  the  heart  participate  in  the  excitability.  It  is  not  due  merely  to  a 
dilatation  of  the  heart,  for  we  may  have  hearts  greatly  dilated  that  show  no 
marked  rapidity  of  action,  and  there  may  be  hearts  of  normal  size  which  may 
for  a  long  time  beat  with  great  rapidity.  Apart  from  the  neurotic  cases,  it 
might  be  assumed  that  an  intoxication  of  the  heart,  or  a  deficiency  in  some 


Fig.  71.  Simultaneous  tracings  of  the  radial  and  jugular  pulses.  The  rhythm  is  normal, 
the  rate  164  per  minute.  There  is  an  auricular  extra-systole  (a'  and  c'  in  the  jugular  tracing 
and  r'  in  the  radial). 

nutriment,  is  the  fundamental  cause  that  renders  the  tissues  more  irritable. 
That  the  whole  tissue  is  involved,  and  not  merely  the  cardiomotor  centre, 
is  demonstrated  in  many  cases  by  the  quicker  contraction  of  the  chambers 
and  the  accelerated  conduction  of  the  stimulus  from  auricle  to  ventricle. 
Thus,  in  Fig.  71  the  tracing  shows  a  very  minute  a-c  interval,  while  notwith- 
standing the  abnormal  rapidity  of  the  heart's  action,  the  excitability  of 
the  auricular  muscle  was  so  great  that  a  premature  auricular  systole  actually 
appeared. 

§  131.  Prognosis. — A  number  of  people  whose  hearts  beat  too  fre- 
quently show  no  sign  of  heart  trouble.  We  then  can  gauge  their  condition 
by  their  reserve  force.  Apart  from  cases  with  a  previous  rheumatic 
history,  or  of  serious  heart  mischief,  I  have  found  that  people  with  con- 
tinuous rapid  hearts  gradually  recover  so  far  as  the  heart's  condition  is  con- 
cerned, and  even  cases  of  exophthalmic  goitre  may  gradually  recover  with 
the  heart  slowing  down.     If  an  alcoholic  will  but  mend  his  ways  before 


INCREASED  FREQUENCY  OF  THE  HEART'S  ACTION       137 

he  has  induced  organic  changes  in  his  other  organs,  the  heart  shows  a  won- 
derful power  of  recovery.  Manifestly,  in  the  other  ailments,  as  tubercular 
and  mahgnant  diseases,  the  future  progress  of  the  case  is  to  a  certain  extent 
independent  of  the  heart  affection.  I -do  not  like  the  continued  rapidity 
in  cases  with  valvular  lesions,  as  it  implies  a  serious  impairment  of  the 
myocardium,  and  if  they  do  not  respond  to  treatment  they  generally 
speed  on  to  a  fatal  issue. 


CHAPTER   XVI 

Diminished  Frequency  of  the  Heart's  Action 

§  132.   Definition  of  the  term  '  bradycardia  '. 
133.    Normal  bradycardia. 

§  132.  Definition  of  the  term  '  bradycardia  ' — The  term  '  brady- 
cardia '  has  been  used  when  the  arterial  pulse  was  slow,  and  from  this  it  has 
been  inferred  that  the  whole  heart  was  slow  in  its  action.  The  result  of 
this  usage  has  been  to  employ  the  term  in  many  cases  quite  inappro- 
priately. Thus  it  is  most  commonly  used  in  association  with  the  condition 
known  as  '  heart-block  ',  a  condition,  as  will  be  shoAvn  later,  where  the 
ventricle  alone  beats  slowly,  the  auricle  pursuing  a  normal  or  even 
accelerated  rate. 

In  order  to  differentiate  between  the  different  forms  of  slow  pulse-rate, 
it  is  necessary  to  make  observation  of  the  movements  of  the  various  chambers 
of  the  heart.  If  this  is  done,  it  will  be  found  that  the  cases  of  diminished 
frequency  of  the  pulse  can  be  divided  into  four  classes  :  (1)  Those  where 
all  the  chambers  of  the  heart  participate  in  the  slow  action  (normal  brady- 
cardia) ;  (2)  where  the  slow  pulse-rate  is  due  to  a  missed  beat,  the  ventricle 
having  contracted,  the  resulting  pulse-wave  being  too  feeble  to  reach  the 
wrist  (described  in  §  142,  Figs.  85  and  86)  ;  (3)  certain  cases  of  nodal 
rhythm  where  the  auricle  has  ceased  to  beat,  or  does  so  synchronously  with 
the  ventricle  (nodal  bradycardia  described  in  Appendix  IV,  p.  337)  ;  (4) 
where  the  stimulus  is  blocked  between  auricle  and  ventricle  so  that  the 
auricle  beats  at  its  normal  rhythm,  and  the  ventricle  does  not  respond 
to  the  auricular  systole,  but  pursues  an  independent  and  slow  rhythm 
(heart-block,  described  in  §  168,  Figs.  122  and  123)  ;  (5)  where  the  vagus 
slows  the  heart,  producing  standstill  of  the  whole  heart  for  irregular  periods 
(p.  24). 

§  133.  Normal  bradycardia — This  only  occurs  when  all  the  chambers 
of  the  heart  participate  in  the  slow  action.  The  demonstration  of  the 
character  of  the  slowing  is  best  shown  by  tracings  of  the  jugular  pulse 
with  the  radial  (Fig.  48,  p.  113)  or  apex  beat  (Fig.  72,  p.  139),  where  the 
auricle  is  seen  to  beat  at  the  same  rate  as  the  ventricle.     I  have  never 


DIMINISHED  FREQUENCY  OF  THE  HEART'S  ACTION      139 

found  this  form  of  slow  heart  beating  under  forty  per  minute,  though  some- 
times we  meet  with  single  pauses  lasting  nearly  two  seconds  (Fig.  79,  p.  146). 
There  is  a  number  of  people  in  the  enjoyment  of  perfect  health,  whose 
pulse  beats  regularly  about  fifty  per  minute.  Those  of  whom  I  have  kept 
a  record  were  mostly  tall  men.  In  a  great  many  people  of  spare  habit, 
who  suffer  also  from  the  X  disease  (§  65),  the  heart-rate  may  fall  under 
fifty  beats  per  minute.  In  some  of  these  a  rise  of  temperature  of  one  or 
two  degrees  may  actually  make  the  pulse  beat  slower.  There  are  other 
conditions  which  may  induce  a  slowing  of  the  heart's  pulse,  such  as  increased 
arterial  pressure  in  Bright's  disease,  in  gout,  and  in  certain  cases  of  arterial 


Fig.  72.     Simultaneous  tracings  of  the  jugular  pulse  and  apex  beat,  showing  the  participa- 
tion of  auricle  and  ventricles  in  true  bradycardia.     Rate  50  per  minute. 


degeneration.  In  pregnancy  the  pulse  may  also  be  occasionally  slow. 
Jaundice  is  said  to  have  a  considerable  power  in  slowing  the  pulse,  but 
I  myself  have  never  found  it. 

Occasionally  we  find  patients  losing  their  memory,  and  the  pulse  will 
be  found  to  be  very  slow — between  forty  and  fifty  beats  per  minute.  Further, 
certain  phases  of  respiration  may  slow  the  pulse,  and  also  the  exposure  of 
the  body  to  the  cold  air  or  to  cold  baths.  So  far  as  I  have  observed,  I  have 
never  found  any  serious  result  from  such  slowing  of  the  heart,  and  I  have 
watched  patients  whose  pulse  may  frequently  be  found  about  fifty  per 
minute,  for  fifteen  and  twenty  years. 


CHAPTER   XVII 

The  Irregular  Action  of  the  Heart 

§  134.     Places  where  the  heart's  contraction  may  start. 
135.     Classification  of  irregularities. 

Irregular  action  of  the  heart  is  of  importance  in  indicating  the  mechan- 
ism of  many  of  the  heart's  actions,  and  a  knowledge  of  this  mechanism  is 
essential  to  the  proper  diagnosis  of  pathological  changes.  As  it  is  a  subject  of 
some  complexity,  I  give  in  this  chapter  a  brief  review  of  the  more  important 
points  bearing  upon  irregular  rhythm,  and  a  classification  of  the  more 
common  forms. 

Irregularities  are  of  such  great  frequency,  and  their  presence  so  readily 
recognized  by  both  patient  and  physician,  that  it  is  necessary  clearly  to 
recognize  their  meaning  and  significance.  Until  a  few  years  ago  their  nature 
was  shrouded  in  obscurity,  and  in  consequence  the  mystery  regarding 
them  in  a  great  measure  oppressed  both  patient  and  physician.  The  fact 
that  in  some  instances  irregularity  was  of  serious  import  led  to  the  sup- 
position that  all  irregularities  are  signs  ©f  some  grave  mischief.  In  con- 
sequence of  this  many  patients  are  subjected  to  unnecessary  fears,  made  to 
carry  out  elaborate  methods  of  treatment,  and  have  imposed  upon  them 
burdensome  and  unnecessary  restrictions. 

The  advance  that  has  been  made  in  the  knowledge  of  this  subject  within 
recent  years  positively  constitutes  a  revolution.  By  the  combined  efforts 
of  clinicians  and  experimental  physiologists,  what  was  recently  a  complete 
mystery  is  now  one  of  the  best  understood  matters  in  the  whole  science  of 
medicine.  Not  only  has  the  scientific  aspect  been  followed  out  thoroughly, 
but  by  watching  individual  cases  for  years  and  noticing  the  changes  that 
have  taken  place  with  advancing  years,  and  observing  how  people  with 
irregular  hearts  have  borne  the  stress  of  life,  I  have  endeavoured  to  obtain 
a  clearer  conception  of  the  bearing  of  the  different  irregularities  upon  the 
future  history  of  the  patient. 

§  134.  Places  where  the  heart's  contraction  may  start. — The  start- 
ing-place of  the  heart's  contraction  is  in  the  remains  of  the  sinus-venosus 
that  have  been  incorporated  in  the  veins,  such  as  the  node  of  tissue  described 


THE  IRREGULAR  ACTION  OF  THE  HEART  141 

by  Keith  and  Flack  at  the  mouth  of  the  superior  vena-cava  (1,  Fig.  2,  p.  15). 
In  describing  the  functions  of  the  primitive  cardiac  tube  (of  which  the 
above-mentioned  node  is  a  portion)  it  was  pointed  out  that  any  part  of  the 
structure  was  capable  of  starting  the  contraction,  and  that  it  was  because 
the  venous  end  was  the  more  excitable  that  the  normal  rhythm  started 
there  (p.  12).  When  another  part  of  this  primitive  tube  becomes  from 
any  cause  more  excitable  than  the  sinus  portion,  then  the  contraction 
starts  at  that  more  excitable  part,  and  an  abnormal  rhythm  results.  If 
a  break  should  occur  in  the  extension  of  the  primitive  tissue,  the  two  divi- 
sions of  the  heart  will  beat  separately  and  independently,  as  is  shown  in 
the  Stannius'  ligature  (p.  13).  In  what  is  called  '  heart-block '  such 
a  separation  occurs,  and  auricle  and  ventricle  beat  at  independent  rhythms. 
For  practical  purposes,  we  can  therefore  reasonably  assume  four  places 
where  the  contraction  of  the  human  heart  can  start  : — 

(a)  At  the  mouth  of  the  great  veins  where  the  remains  of  the  sinus 
venosus  still  persist,  giving  rise  to  the  normal  or  sinus  rhythm.  (6)  At 
the  a.-v.  node,  where  auricle  and  ventricle  contract  simultaneously,  (c)  In 
the  a.-v.  bundle  on  the  ventricular  side  of  the  a.-v.  node,  where,  while  the 
auricle  contracts  in  obedience  to  the  sinus  rhythm,  the  ventricle  contracts 
independently,  {d)  In  the  auricular  tissue,  where  some  part  of  the  primi- 
tive tube  seems  to  persist. 

§  135.  Classification  of  irregularities. 

(1)  Sinus  irregularities. — The  heart's  contraction  arising  normally  in 
the  remains  of  the  sinus  venosus  is  set  to  a  regular  rhythm.  The  sinus 
tissue  may  be  excited  or  depressed  as  by  nerve  influence,  and  irregularities 
may  then  occur.  This  form  of  irregularity  is  characterized  by  a  varying 
length  of  the  cardiac  cycle,  mainly  of  the  diastoUc  portion,  the  pidse  beats 
being  always  of  equal  size  or  nearly  equal  size,  and  presenting  no  '  imper- 
fect systoles  '  or  '  missed  beats  '.  The  variation  usually  corresponds  with 
certain  phases  of  respiration.  It  is  most  frequent  in  the  young,  but  is 
occasionally  present  in  adult  life  (see  Chapter  XVIII). 

(2)  Extra-systoles. — Here  an  auricular  or  ventricular  systole,  or  both 
together,  may  start  prematurely  and  independently  of  the  sinus  rhythm. 
They  occur  occasionally  in  an  otherwise  regular  heart ;  a  premature  beat 
of  the  radial  pulse  is  felt,  followed  by  a  long  pause,  or  there  may  simply 
be  a  long  pause  (intermittent  pulse).  Sometimes  these  extra-systoles  may 
occur  with  greater  frequency,  even  every  second  beat  being  of  this  nature 
(pulsus  bigeminus).  When  they  are  so  small  as  to  be  imperceptible  to  the 
finger,  it  might  seem  as  if  the  heart  were  beating  extremely  slowly.  On  aus- 
cultation synchronous  with  the  premature  beat,  two  short,  sharp  sounds  are 


142  DISEASES  OF  THE  HEART 

heard — the  first  and  second  sound  of  the  premature  or  extra-systoHc  contrac- 
tion.  These  sounds  are  very  characteristic  of  this  condition  (Chapter  XIX). 

(3)  Nodal  rhythm. — In  advanced  disease  of  the  heart  from  rheumatism 
and  cardio-sclerosis,  the  starting-place  of  the  contraction  is  no  longer  at 
the  sinus,  but  in  some  part  lower  down,  where  the  auricle  and  ventricle 
are  stimulated  to  contract  for  the  most  part  simultaneously.  Beats  of 
varying  size  follow  one  another  at  varying  intervals  ;  sometimes  the  irregu- 
larity is  extreme,  sometimes  scarcely  perceptible,  but  careful  analysis  will 
usually  show  variations  in  the  length  of  the  cardiac  cycle.  This  irregularity 
is  usually  associated  with  marked  diminution  of  the  heart's  power,  sometimes 
extreme,  at  other  times  only  indicated  by  a  limitation  of  the  field  of  cardiac 
response  when  the  patient  makes  an  effort.  It  may  occur  at  all  ages.  The 
heart's  rate  is  as  a  rule  more  frequent  than  normal  and  it  may  be  extremely 
rapid  temporarily  (paroxysmal  tachycardia)  or  continuously  ;  when  con- 
tinuously rapid,  it  may  slow  down  and  beat  about  seventy  to  ninety  per 
minute.  In  some  cases  it  is  less  frequent  than  normal  (nodal  bradycardia, 
p.  337). 

(4)  Irregularities  due  to  failure  of  the  conducting  power  of  the  primitive 
bundle. — This  is  due  to  the  ventricular  systole  dropping  out  in  consequence 
of  the  stimulus  for  contraction  not  reaching  the  ventricle.  This  condition 
is  rare,  but  may  occasionally  occur  in  influenza  and  other  infectious  com- 
plaints, and  in  old  and  recent  rheumatic  hearts,  especially  after  digitalis,  and 
in  cardio-sclerosis.  A  more  extreme  form  of  the  condition  is  known  as 
heart-block.  This  condition  may  be  suspected  when  there  is  a  complete 
pause  in  the  radial  pulse  with  absence  of  heart  sounds  (Chapter  XXI). 

(5)  Depression  of  contractility  {pulsus  alternans). — Irregularities  due  to 
the  failure  of  the  contractile  power  of  the  ventricle  are  usually  regular 
in  rhythm — the  beats  varying  in  strength  only.  The  most  common  form 
is  that  where  a  strong  beat  alternates  with  a  weak,  the  rate  being  quite 
regular  (Chapter  XXII,  §  179). 


CHAPTER   XVIII 


Sinus  Irregularities 

§  136.  Character  of  the   u'regularity. 

137.  Etiology. 

138.  Symptoms. 

139.  Associated  symptoms. 

140.  Prognosis. 

§  136.  Character  of  the  irregularity. — As  the  primitive  cardiac  tissue 
at  the  mouth  of  the  great  veins  possesses  in  a  degree  higher  than  any 
other  part  the  power  of  rhythmically  producing  the  stimulus  for  con- 
traction, the  rhythm  of  the  whole  heart  follows  normally  the  time  set  by 
this  portion  of  the  primitive  tissue.  While  normally  this  rhythm  is  a 
fairly  regular  one,  as  a  matter  of  observation  we  find  a  great  many  people 
who  show  a  variation,  sometimes  slight,  sometimes  marked,  in  the  duration 


Fig.  73.  Simultaneous  tracings  of  the  jugular  and  radial  pulses,  showing 
the  agreement  in  rhythm  of  the  right  auricle  and  ventricle  (waves  a  and  v)  with 
the  radial  pulse,  in  the  sinus  form  of  irregularity.  The  irregularity  is  seen  to  be 
due  to  variations  in  the  length  of  the  diastoUc  period  (spaces  O). 

of  the  cardiac  cycle.  There  is  a  much  greater  constancy  in  the  duration  of 
the  systolic  period  of  the  cardiac  cycle  than  of  the  diastolic.  With  the 
quickening  of  the  pulse-rate,  the  shortening  of  the  period  of  the  cardiac 
cycle  takes  place  almost  entirely  at  the  expense  of  the  diastolic  portion. 
In  sinus  irregularities  it  is  the  variation  in  the  length  of  the  diastolic  period 
that  is  the  chief  characteristic.  In  the  quickened  pulse  we  find  the  duration 
of  the  diastolic  period  reduced,  so  that  with  increase  of  rate  this  irregularity 
disappears.  On  the  other  hand,  when  the  heart  gradually  slows  in  its  action 
this  form  of  irregularity  is  prone  to  occur,  so  that  we  find  it  best  in  the  young 
and  in  some  adults  after  a  febrile  attack  or  during  slow  respiration.  Typical 
instances  of  sinus  irregularity  are  given  in  Figs.   73  and  74.     In  Fig.  73 


144  DISEASES  OF  THE  HEART 

the  irregularity  is  seen  to  be  due  to  variations  in  the  length  of  the  diastole 
of  the  heart  (period  O),  the  systolic  period  (E)  remaining  constant.  The 
jugular  tracings  show  that  the  right  auricle  (a)  and  ventricle  (v)  participate 
in  the  same  irregularity  as  the  radial  pulse. 

§  137.  Etiology. — It  is  generally  agreed  that  this  irregularity  is  of 
vagus  origin.  Normally  there  is  a  certain  degree  of  inhibition  maintained 
by  this  nerve,  but  its  centre  may  become  unusually  susceptible  to  impulses 
from  other  parts,  and  these  are  transmitted  reflexly  to  the  heart.  This  is 
well  seen  in  some  cases  where  the  vagus  is  more  excitable.  In  certain  cases 
the  reflex  stimulation  of  the  vagus  will  produce  an  alteration  of  the  heart's 
rate,  as  in  Fig.  75,  Plate  I,  where  it  is  shown  that  the  act  of  swallowing 
quickened  the  heart-rate  for  a  few  beats,  and  then  caused  a  slowing. 
A  more  striking  illustration  of  the  reflex  effect  of  swallowing  on  the  heart 
is  found  in  Figs.  258  and  259,  Plate  IV,  where  it  not  only  slowed  the  sinus 


Fig.  74.  Simultaneous  tracings  of  the  jugular  and  radial  pulses,  showing  that  the  auricle 
participates  in  the  irregularity,  and  that  there  is  no  premature  contraction  during  the  long 
pauses  (sinus  irregularity). 

rhythm,  but  depressed  the  conductivity  of  the  a. -v.  fibres,  so  that  the 
stimulus  from  auricle  to  ventricle  was  occasionally  blocked.  In  Fig.  76, 
Plate  I,  a  vagus  effect  is  shown  after  the  patient  has  taken  three  deep 
and  hurried  respirations.  This  patient  was  under  the  influence  of  digitalis, 
but  here  the  effect  is  purely  upon  the  sinus,  showing  a  slowing  of  the  rate. 
In  these  tracings  it  is  further  to  be  noted  that  the  vagus  effect  is  not 
immediately  produced  and  does  not  at  once  pass  off,  but  lasts  some  little 
time.  Thus,  in  Figs.  75,  Plate  I,  258  and  259,  Plate  IV,  there  is  shown 
a  secondary  slowing  some  seconds  after  the  swallowing,  and  in  Fig.  76, 
Plate  I,  the  slowing  comes  gradually  on  after  the  hurried  respirations.  The 
reason  I  dweU  upon  this  is  because  this  sinus  arrhythmia  is  often  distinctly 
respiratory  in  origin,  though  the  pulse  variations  do  not  always  correspond 
with  identical  phases  of  the  respiration,  as  in  Fig.  77,  Plate  II,  where  the 
slowing  occurs  at  different  phases  of  the  respiratory  movement. 

In  the  dog  this  irregularity  is  very  common,  and  disappears  on  section 
of  the  vagus.  An  irregularity  identical  with  Fig.  79,  due  to  vagus  stimu- 
lation, is  shown  in  Fig.  78. 


SINUS  IRREGULARITIES 


145 


§  138.  Symptoms — This  irregularity  is  easily  recognized.  To  the 
finger  the  pulse-rate  is  continually  changing,  usually  with  respiration,  and 
the  beats  are  equal  in  strength.  On  auscultation  the  sounds  are  heard 
clear  and  distinct,  and  the  interval  between  the  first  and  second  sounds  is 
constant.  By  the  ear,  the  varying  difference  in  the  diastolic  period  can  be 
made  out  more  easily  than  by  the  pulse.  In  rare  instances  the  slowing 
may  occur  at  rare  intervals  and  affect  only  one  or  two  beats,  as  in 
Fig.  79,  and  there  may  be  at  first  some  difficulty  in  recognizing  the 
nature  of  the  irregularity,  but  when  the  condition  of  the  patient  in  other 


Fig.  78.  Shows  the  effect  of  vagus  stimulation  in  the  dog's  heart.  The  down- 
ward movements  in  the  tracing  of  auricle  and  ventricle  are  due  to  the  systole. 
The  vagus  was  stimulated  at  s,  and  produced  a  standstill  of  the  whole  heart 
(Cushny). 

respects  is  taken  into  account,  the  nature  of  the  irregularity  can  be 
inferred  with  certainty.  Such  an  irregularity  from  any  other  cause  would 
show  evidence  of  severe  heart  trouble  (as  heart-block  or  the  nodal 
rhythm),  whereas  in  such  cases  there  is  no  evidence  of  heart  trouble,  or 
but  the  very  slightest.  Tracings  of  the  jugular  pulse  at  once  determine  the 
nature  of  the  irregularity,  by  showing  that  the  auricle  is  also  subject  to  the 
same  influence. 

§  139.   Associated    symptoms — These    are    merely    incidental,    the 

MACKENZIE  T 


146 


DISEASES  OF  THE  HEART 


irregularity  itself  causing  no  subjective  symptom.  When  some  incidental 
phenomenon  such  as  syncope  appears,  an  undue  importance  may  be  attached 
by  the  physician  to  the  irregularity.  Many  young  folks  have  syncopal 
attacks,  and  this  irregularity,  being  the  only  abnormal  feature  found  by 
the  physician,  is  often  the  ground  on  which  unnecessary  alarm  and 
unnecessary  treatment  are  based. 

Although  in  the  vast  majority  of  cases  the  slowing  of  the  heart, 
presumably  due  to  vagus  action,  gives  rise  to  no  symptoms,  particularly 
in  the  young  and  when  of  respiratory  origin,  yet  the  period  of 
standstill  may  be  at  times  so  long  as  to  produce  an  effect  on  the 
brain.  The  patient  from  whom  Fig.  79  was  taken  had  attacks  of 
giddiness  at  times,  and  the  pauses  in  the  heart's  action  were  often  longer 


Fig.  79.  Occasional  slowing  of  the  Avhole  heart  due  to  inhibitory  nerve  influences  on  the 
sinus.     The  a-c  interval  (space  A)  is  not  affected  by  the  variations  in  rate.     (Compare  with 

Fig.  78.) 

than  that  figured  here.  Laslett  ^^^  records  a  case  and  gives  numerous 
tracings  in  which  the  standstill  was  frequently  so  long  that  the  patient 
lost  consciousness. 

In  the  vague  condition  which  I  have  described  as  the  X  disease  (§  65) 
the  respirations  are  often  slow,  falling  sometimes  to  seven  per  minute.  When 
this  occurs,  the  pulse  invariably  shows  this  irregularity  (Fig.  77,  Plate  II). 
It  has  also  been  found  present  in  neurasthenia,  and  some  go  so  far  as  to 
diagnose  neurasthenia  by  this  irregularity  alone.  Nicholson  '^^*  has  demon- 
strated its  presence  in  infants,  Watson  WiUiams  -^^  in  healthy  schoolboys, 
and  Deane  ^^^  in  athletic  soldiers,  and  I  have  found  it  in  a  great  number  of 
healthy  individuals,  so  that  one  can  safely  look  upon  its  association  with 
neurasthenia  as  merely  incidental.  It  is  this  form  of  irregularity  which 
is  present  in  tubercular  meningitis. 

§  140.  Prognosis. — There  is  no  reason  for  attaching  importance  to 
this  irregularity,  and  no  condition  should  be  considered  more  grave 
because  of  its  presence.     After  a  febrile  attack  it  may  usually  be    looked 


SINUS  IRREGULARITIES  147 

upon  as  a  favourable  sign.  Its  presence  in  tubercular  meningitis  adds 
nothing  to  the  seriousness  of  the  condition. 

The  presence  of  this  sinus  irregularity  may  even  afford  grounds  for 
a  favourable  prognosis  when  it  occurs  in  the  young  after  recovery  from 
rheumatic  fever,  even  though  there  may  be  a  mitral  systolic  murmur, 
for  it  is  not  present  when  there  is  exhaustion  of  the  heart  muscle. 

Treatment. — It  calls  for  no  special  treatment,  nor  should  any  attempt 
be  made  to  treat  this  symptom  alone. 


l2 


CHAPTER   XIX 

The  Extra-systole 

§  141.  Definition  of  the  term  '  extra-systole  '. 

142.  Character  of  the  irregularity. 

143.  Etiology. 

144.  Ventricular  extra-systole. 

145.  Auricular  extra-systole. 

146.  Nodal  extra-systole. 

147.  Condition  of  the  a.-v.  bundle  in  cases  showing  extra-systoles. 

148.  The  dropping  out  of  the  beat  after  the  extra-systole. 

149.  Reasons  for  attributing  the  origin  of  extra-systoles  to  affections 

of  the  remains  of  the  primitive  cardiac  tube. 

150.  Conditions  inducing  extra-systoles. 

151.  Sensations  produced  by  extra-systoles. 

152.  Prognosis. 

153.  Treatment. 

§  141.  Definition  of  the  term  *  extra-systole  ' There  are  so  many 

conditions  that  simulate  extra-systoles,  that  a  good  deal  of  confusion  exists 
in  regard  to  what  really  constitutes  an  extra-systole,  and  it  is  therefore 
necessary  to  define  the  term.  As  the  stimulus  for  contraction  arises  normally 
in  the  remains  of  the  sinus  venosus  at  the  mouths  of  the  great  veins,  and  as 
the  stimulus  passes  from  these  places  to  the  auricle,  then  to  the  ventricle, 


Fig.  80.     The  small  beats  are  due  to  extra-systoles. 

80  that  there  is  normally  a  sequence  of  stimulation  and  contraction  of  sinus, 
auricle,  and  ventricle,  I  would  suggest  that  the  term  '  extra-systole  '  should 
be  limited  to  those  premature  contractions  of  auricle  or  ventricle  in  response 
to  a  stimulus  from  some  abnormal  point  of  the  heart,  but  where  otherwise 
the  fundamental  or  sinus  rhythm  of  the  heart  is  maintained. 

§  142.    The    character    of    the   irregularity The   extra-systole    is 

usually  recognized  by  the  occurrence  of  a  premature  beat  in  the  radial 
pulse  followed  by  an  abnormally  long  pause,  as  is  shown  in  Fig.  80,  where 


THE  EXTRA-SYSTOLE 


149 


the  two  small  beats  are  extra-systoles.  It  may  appear  only  at  rare  intervals, 
or  it  may  occur  at  frequent  irregular  intervals,  or  regularly  after  every 
1,  2,  3,  4,  or  more,  normal  beats,  as  in  Figs.  81,  82,  83,  84. 


Fig.  81.    Pulsus  bigeminus  due  to  an  extra-systole  occurring  after  each  normal  beat. 


Fig.  82.     Extra-systole  occurring  after  every  two  normal  beats. 


Fig.  83.     Extra-systoles  occurring  after  every  three  normal  beats. 


Fig.  84.     Extra-systoles  occurring  after  every  four  normal  beats. 

The  ventricular  contraction  causing  the  extra-systole  may  be  so  weak 
that  no  wave  is  perceptible  to  the  finger  in  the  radial,  though  it  may  be 
detected  in  the  sphygmogram,  as  in  Fig.  85.  In  some  cases  it  may  even 
not  appear  in  the  sphygmogram,  but  the  heart's  sounds,  or  a  tracing  of  the 
apex  beat  at  the  same  time,  show  that  during  the  long  pause  in  the  radial 
pulse  the  ventricle  contracted,  but  not  with  sufficient  strength  to  send  a  wave 
into  the  radial  artery  (Fig.  86). 

In  these  cases  the  pulse  is  described  as  '  intermittept  *,  or,  if  the  extra- 


150 


DISEASES  OF  THE  HEART 


systoles  occur  regularly  after  each  normal  beat,  the  pulse  at  the  wrist  appears 
extremely  slow,  and  the  case  may  be  put  down  as  '  bradycardia  ',  or  heart- 
block.  It  may  be  differentiated  by  the  observation  of  the  jugular  pulse  or 
apex  beat,  or  by  auscultation. 


Fig.  85.     Slow  pulse  feeling  to  the  finger  about  30  per  minute.     The  small  waves  (r')  are 
due  to  extra- systoles  and  were  not  perceptible  to  the  finger. 

The  extra-systole  is  easily  recognized  on  auscultation.      The  regular 
sequence  of  sounds  is  interrupted  by  two  short,  sharp  sounds  (if  very  feeble, 


Apex  'beat 

^r\  r\r\ 

Af\          n  y^ 

r\n 

yuV^ 

^\l^n 

y  n 

r-f- 

-J^^-^-J^ 

~JM 

Radial 

Fig.  86.    Simultaneous  tracings  of  the  apex  beat  and  of  the  radial 
pulse.     There  are  two  beats  of  the  apex  to  one  radial  pulse. 

only  one  sound  may  be  heard)  followed  by  a  long  pause,  as  is  represented 
in  the  diagrams,  Figs.  87  and  88. 

iiiiaiMiB 

Fig.  87.     Diagram  representing  the  sounds  of  the  heart 
with  occasional  extra-systoles. 

§  143.  Etiology. — In  seeking  for  an  explanation  for  the  occurrence  of 
extra-systoles,  I  collected  a  large  number  of  instances  and  then  sought 
for  some  basis  of  classification.  Hitherto  the  classification  has  to  a  great 
extent  been  based  on  the  results  of  experiments,  but  I  found  in  the  human 


THE  EXTKA-SYSTOLE  151 

heart  many  variations  which  did  not  coincide  with  experimental  results. 
After  trying  various  methods,  I  took  up  the  idea  that  the  remains  of  the 
primitive  cardiac  tube  in  the  human  heart  might  preserve  the  functional 
peculiarities  of  the  original  tube.  One  of  these  peculiarities  is  the  power 
possessed  by  any  part  of  the  tube,  if  rendered  more  excitable,  to  start  the 
heart's  contraction  before  the  sinus.  As  the  primitive  tube  in  the  heart  is 
represented  at  the  mouths  of  the  great  veins,  in  the  auricle,  in  the  a.-v.  node, 
and  in  the  a.-v.  bundle  after  it  leaves  the  node  (Fig.  2),  I  reasoned  that  while 
the  normal  rhythm  started  at  the  veins,  premature  contractions  might 
start  in  the  remains  in  the  auricle,  a.-v.  node,  or  bundle.  Examining  my 
tracings  with  this  view  in  mind,  I  found  that  the  vast  majority  readily 
fell  into  this  classification. 

A  further  proof  was  found  in  the  fact  that  in  many  cases  the  power 
of  conduction  in  the  a.-v.  bundle  was  impaired,  implying  an  invasion  of 
this  system  by  the  disease,  a  view  further  supported  by  post-mortem 
examinations. 


Fig.  88.  Diagrammatic  representation  of  the  sounds  of  the 
heart  in  a  case  of  such  rhythmical  irregularity  as  is  represented  in 
Figs.  81,  85,  and  86. 

Wliile  I  do  not  assert  that  this  view  is  proven  to  be  correct,  I  use  it, 
as  it  brings  out  more  clearly  the  salient  points  of  the  varied  forms  of 
extra-systole,  I  claim  no  originality  for  this  suggestion,  as  the  possibility 
of  arrhythmias  arising  at  the  a.-v.  bundle  has  occurred  to  many  people. 

§  144.  Ventricular  extra-systole — (The  place  of  origin  of  ventri- 
cular extra-systoles  is  assumed  to  be  in  the  a.-v.  bundle  beyond  the  a.-v. 
node  or  in  some  part  of  its  branches  in  the  ventricular  wall.)  The  simplest 
form  of  extra-systole  is  that  where  a  premature  contraction  of  the  ventricle 
is  interpolated  between  two  normal  beats. 

In  Fig.  89  there  are  two  small  waves  r'  in  the  radial,  which  are  due  to 
extra-systoles  of  the  left  ventricle.  In  the  tracing  from  the  neck  the  waves 
c  are  due  to  the  carotid,  the  waves  a  are  due  to  the  auricle,  and  the  waves  c' 
are  due  to  the  extra-systoles  and  correspond  to  r'  in  the  radial.  The  diagram 
intercalated  between  the  radial  tracing  and  the  tracing  from  the  neck 
shows  the  relationship  of  the  different  events.  The  downstrokes  in  the 
upper  compartment  represent  the  beginning  of  the  auricular  systoles,  and 
the  downstrokes  in  the  lowest  compartment  represent  the  beginning  of  the 


152 


DISEASES  OF  THE  HEART 


carotid  pulse  beats,  while  the  slanting  lines  in  the  middle  compartment 
represent  the  time  between  the  beginning  of  the  auricular  and  carotid 
waves  (the  a-c  interval).  In  the  cardiac  cycles,  apart  from  those  in  which 
the  extra-systoles  r'  and  c'  occur,  the  ventricular  contraction  follows 
regularly  on  the  auricular,  and  it  is  assumed  that  the  sinus  rhythm  governs 
the  contraction  of  the  auricle.  The  extra-ventricular  contractions  are  seen 
to  start  independently  of  the  auricular  contraction — that  is,  they  are  extra- 
systoles  of  the  ventricle.  The  same  features  are  to  be  recognized  in  Fig.  90, 
Plate  II,  where  there  are  four  extra-systoles  (r'  in  the  radial,  and  c'  in  the 
jugular  tracing)  ;   it  will  be  seen  that  the  auricular  wave  appears  at  regular 


Fig.  89.  Simultaneous  tracing  of  the  jugular  and  radial  pulses,  showing  the  interpolation 
of  ventricular  extra-systoles  (c',  c'  and  r',  r')  represented  in  the  diagram  by  the  downstrokes  -f-  -t-. 
The  downstrokes  in  the  space  As  represent  the  auricular  waves  (o)  in  the  jugular,  and  the 
downstrokes  in  the  space  Vs  represent  the  carotid  waves  c,  and  the  slanting  lines  connecting 
them  represent  the  a-c  interval. 


intervals,  and  that  the  extra-systoles  are  interpolated  between  two  normal 
beats. 

In  Fig.  91,  Plate  II,  there  is  an  extra-systole  during  each  of  the  irregular 
periods  B  and  C.  In  the  jugular  tracing  the  carotid  wave  c  follows  the 
auricular  wave  a,  but  during  the  two  irregular  periods  the  carotid  wave  c' 
precedes  the  auricular  wave  a',  a  fact  brought  out  clearly  in  the  intercalated 
diagram.  We  can  prove  that  c'  is  due  to  the  carotid,  because  it  occurs 
at  the  same  time  after  the  preceding  carotid  wave  that  the  radial  beat  r' 
appears  after  the  preceding  radial  beat.  The  auricular  wave  a'  appears  at 
the  normal  auricular  interval,  and  the  auricle  pursues  its  wonted  regular 
rhythm  while  the  ventricle  is  contracting  prematurely  and  independently. 

In  the  irregular  period  B  the  interval  between  a'  and  the  following  c  is 
greatly  lengthened  (space  A^).  The  reason  of  this  delay  is  shown  in  the 
diagram  to  be  due  to  slower  passage  of  the  stimulus  from  auricle  to  ventricle 


THE  EXTRA-SYSTOLE 


153 


— a  fact  of  great  importance,  which  will  be  dealt  with  in  discussing  the 
condition  of  the  conductivity  of  the  auriculo-ventricular  bundle. 

In  the  irregular  period  (7,  there  is  a  much  longer  pause  in  the  radial 
tracing  after  the  extra-systole  r',  and  the  intercalated  diagram  shows  that 
this  is  due  to  the  fact  that  the  ventricle  does  not  respond  to  a  stimulus 
after  a'.  The  difference  between  the  irregular  periods  B  and  C  is  seen, 
therefore,  to  be  due  to  the  fact  that  in  the  irregular  period  B  the  ventricle 
responds  to  the  stimulus  from  the  auricular  systole  after  the  extra-systole, 
whUe  in  the  ii-regular  period  C  the  ventricle  does  not  respond. 

The  irregular  period  C  represents  the  most  common  form  of  extra- 
systole,  and  its  appearance  in  grapliic  records  is  usually  easily  recognized 
by  the  presence  of  the  long  pause  after  the  premature  beat  r'. 


Fig.  92.  Represents  a  common  form  of  ventricular  extra-systole.  There  is  a  long  pause 
after  the  extra-systole  (r').  In  the  jugular  tracing  and  in  the  diagram  this  is  seen  to  be  due 
to  the  failure  of  the  stimulus  from  the  auricle  (a')  to  provoke  a  ventricular  contraction. 


Thus  Fig.  92  is  a  very  characteristic  example,  and  the  intercalated 
diagram  shows  a  regularly  acting  auricle  and  the  premature  and  independent 
ventricular  contraction  with  no  response  to  the  auricular  systole  after  the 
premature  ventricular  contraction,  which  accounts  for  the  long  pause. 

Simultaneous  occurrence  of  the  normal  auricular  systole  and  of  the 
ventricular  extra-systole. — In  the  illustrations  I  have  given  of  the  ventricular 
extra-systole  (as  in  Figs.  89  and  92),  in  the  jugular  tracing  the  carotid  wave 
c'  was  seen  to  precede  the  auricular  wave  a'.  In  these  instances  the  normal 
rate  was  rather  slow.  In  most  instances,  however,  they  fall  together — the 
auricular  contraction  occurring  during  the  ventricular  contraction.  In 
consequence  of  this  the  auricle  cannot  empty  its  contents  into  the  ventricle, 
and  hence  a  big  wave  is  sometimes  sent  into  the  jugular.  In  patients  with 
a  well-marked  jugular  pulse,  this  is  readily  recognized  by  the  eye.  In 
other  cases  the  jugular  pulsation  is  only  to  be  seen  when  this  big  wave  is 
sent  back. 


154 


DISEASES  OF  THE  HEART 


In  Fig.  93  the  waves  a  and  a'  are  due  to  the  auricular  systole,  and_^occur 
at  regular  intervals.  The  waves  a'  are,  however,  much  larger  than  the 
waves  a,  and  the  reason  for  the  increase  in  size  is  found  in  the  fact  that  at 
that  time  the  ventricle  was  also  in  systole,  causing  the  extra-systole.  ^  In 
Fig.  94  a  simultaneous  record  of  the  apex  beat  and  jugular  pulse  shows 
the  premature  contraction  of  the  ventricle  o  at  the  same  time  as  the  large 


Fig.  93.  Simultaneous  tracings  of  the  jugular  and  radial  pulses.  The  small  beats  x  x  x 
are  extra-systoles.  The  auricle  preserves  its  rhythm  during  the  irregular  periods  in  the  radial 
pulse.'  The  wave  a'  is  the  auricular  wave  during  the  premature  contraction  of  the  left  ven- 
tricle. The  absence  of  the  ventricular  wave  v,  after  the  wave  a',  indicates  that  the  right 
ventricle  had  contracted  early,  evidently  synchronous  with  the  premature  contraction  of  the 
left  ventricle,  the  large  wave  following  a'  being  due  to  stasis. 

auricular  wave  a',  so  that  here  also  we  have  evidence  of  the  simultaneous 
contraction  of  auricle  and  ventricle  during  a  ventricular  extra-systole. 
When  there  is  a  large  jugular  pulse,  the  increased  size  of  the  auricular  wave 
occurring  during  the  extra-systole  of  the  ventricle  may  not  be  so  marked 
as  in  Fig.  95. 


Apexl>eat 


dfp        a  C 


mint.  Jugular 


Fig.  94.  Simultaneous  tracings  of  the  apex  beat  and  of  the  jugular  pulse,  showing  the 
rh3rthmical  appearance  of  the  auricular  wave  during  the  irregular  periods  in  the  apex  tracing. 
The  small  beats  o  o  o  are  extra-systoles  of  the  ventricle. 

§  145.  The  auricular  extra-systole — (The  suggestion  put  forward 
here  is  that,  in  the  production  of  the  auricular  extra-systole  the  stimulus 
arises  in  the  primitive  tissue  incorporated  in  the  auricle— the  exact  site 
being  still  undetermined.) 

When  an  extra-systole  arises  in  the  auricle,  the  sounds  of  the  heart  and 
the  radial  tracing  present  exactly  the  same  features  as  when  a  ventricular 
extra-systole  occurs,  and  it  is  only  by  a  simultaneous  record  of  the  jugular 


THE  EXTRA-SYSTOLE 


155 


pulse  that  the  one  can  be  differentiated  from  the  other.  In  Figs.  96  and  97 
the  radial  pulse  shows  premature  beats  {r'),  which  can  be  readily  identified 
as  extra-systoles. 

In  the  jugular  tracings  the  carotid  wave  c'  is  preceded  by  an  auricular 
wave  a',  and  the  only  inference  that  can  be^drawn  is  that  a'  is  due  to  an 


Fig.  95.  Shows  three  ventricular  extra-systoles  in  the  radial  (r')  while  the  auricle  pursues 
its  regular  rhythm  (o  and  a').  The  downstrokes  3  and  4  represent  the  time  of  the  carotid  and 
radial  pulses. 

extra-systole  of  the  auricle,  which  is  followed  by  an  extra-systole  of  the 
ventricle,  producing  the  carotid  and  radial  beats  c'  and  r'. 

In  such  instances  as  these  the  auricle  is  supposed  to  contract  in  reply  to 
a  stimulus  from  some  source  other  than  the  sinus,  and  the  long  pause  after 
the  extra-systole  is  due  to  the  fact  that  the  stimulus  from  the  sinus  arising  at 


Fig,  96.  Shows  auricular  extra-systoles  (a')  followed  by  ventricular  contractions  (c',  r'). 
The  arrows  in  the  diagram  represent  the  sinus  stimulation  and  the  long  pauses  after  the  extra- 
systoles  are  seen  to  be  due  to  the  fact  that  the  auricle  did  not  respond  to  the  sinus  stimulation. 

its  normal  time  fails  to  provoke  the  refractory  auricle  to  contraction.  This 
is  brought  out  in  the  intercalated  diagram  in  Fig.  96,  in  which,  above  the 
upper  space,  are  arrows  representing  the  sinus  stimulation.  In  the  diagram 
it  mil  be  seen  that  there  is  no  response  to  the  sinus  stimulation  after  the 
extra-systole,  but  that  auricle  and  ventricle  remain  quiescent  till  the  following 


156 


DISEASES  OF  THE  HEART 


sinus  stimulation  excites  them  to  a  contraction.  In  these  two  illustrations 
the  irregular  period  is  equal  to  two  cardiac  cycles,  the  explanation  being 
obvious  from  the  study  of  the  diagram  in  Fig.  96.  In  most  cases  of  auricular 
extra-systole,  the  irregular  period  is  less  than  two  cycles,  as  is  shown  in  Figs. 
98  and  99.     The  reason  given  by  Cushny  ^^^  and  Wenckebach  -^,  and  usually 


Fig.  97.     Shows  an  auricular  extra-systole  a'.     The  numbers  represent  tenths  of  a 
second  and  the  irregular  period  (r')  equals  two  normal  periods. 

accepted,  is  that  the  stimulus  arising  in  the  auricle  passes  back  to  the  sinus 
and  stimulates  the  sinus  so  that  its  stored  energy  is  exhausted,  and  it  begins 
to  build  up  anew  the  stimulus  material.  As  soon  as  it  has  again  reached 
the  excitable  stage,  it  starts  off  the  contraction.      Thus  in  the  diagram 


Fig.  98.  Shows  two  premature  or  extra-systoles  of  auricular  origin  (  x  ).  The  waves  c'  in 
the  jugular  tracing  occur  at  the  same  time  as  the  small  premature  beats  (-f)  in  the  radial 
tracing,  and  are  therefore  due  to  the  carotid.  These  are  preceded  by  premature  waves  o'  due 
to  the  auricle.  The  interval  a'-c'  (space  ^3)  is  greater  than  the  average  a-c  interval  (^2)-  ^'^^ 
is  much  greater  than  the  following  a-c  interval  (A^). 

(Fig.  100),  representing  the  events  in  Fig.  99,  the  stimulus  is  represented 
coming  down  from  the  sinus  to  the  auricle,  but  at  the  extra-systole  ( + ) 
the  stimulus  is  represented  by  an  arrow  passing  back  to  the  sinus,  so  that 
the  sinus  responds  to  the  retrograde  stimulation.  After  this  premature  stimu- 
lation, the  sinus  rests  for  a  normal  period,  and  starts  off  again  at  the  normal 


THE  EXTRA-SYSTOLE 


157 


rhythm.  This  irregular  period,  due  tp  the  auricular  extra-systole,  is  so. 
frequently  shorter  than  two  normal  beats  that  this  is  usually  assumed  to  be 
the  manner  in  which  it  is  brought  about.  While  it  offers  a  plausible  ex- 
planation, it  cannot  be  said  in  any  sense  to  have  been  proved,  and  there  are 
other  possibilities  which  need  consideration  before  it  can  be  finally  accepted. 


Fig.  99.    Shows  an  extra-systole  of  axiricular  origin  at  a'. 

the  diagram,  Fig.  100. 


This  tracing  is  interpreted  in 


As,  however,  they  are  still  speculative,  it  would  not  be  convenient  to  discuss 
them  here. 

§  146.  The  extra-systoles  arising  in  the  auriculo-ventricular 
node  (nodal  extra-systole). — So  far  the  recognition  of  extra-systoles  as 
ventricular  or  aiiricular  has  been  comparatively  easy.  There  is  a  4;hird 
class  which  has  hitherto  not  been  sufficiently  considered,  and  which,  in  my 
opinion,  has  been  wrongly  interpreted.     The  characteristic  feature  of  these 


Fig.  100.  Diagram  representing  the  events  in  Fig.  99.  The  extra-stimulation  at  -f  is 
represented  arising  in  the  auricle,  passing  back  and  disturbing  the  sinus  rhjrthm.  Note  the 
lengthened  a-c  interval  after  the  auricular  extra-systole. 


extra-systoles  is  that  auricle  and  ventricle  contract  prematurely  and  together. 
In  Figs.  93,  94,  and  95,  it  was  demonstrated  that  auricle  and  ventricle  con- 
tracted together  when  the  ventricular  extra-systole  appeared  at  the  same 
time  as  the  normal  auricular  systole.  In  these  cases  the  auricle  could  be 
demonstrated  to  contract  at  its  normal  period.  In  another  class  of  cases 
it  can  be  demonstrated  that  both  auricle  and  ventricle  contract  prematurely 
and  together,  the  auricular  wave  appearing  at  the  same  time  as  the  arterial 


158  DISEASES  OF  THE  HEART 

pulse.  Thus  in  Figs.  101  and  102,  the  auricular  waves  a'  in  the  jugular 
appear  prematurely,  and  obscure  the  appearance  of  the  carotid  waves, — 
the  time  when  the  latter  were  due  can  be  ascertained  by  measuring  the  time 
between  the  extra-systole  in  the  radial  pulse,  and  the  preceding  beat.  That 
the  auricle  did  not  contract  at  its  normal  time  is  evident  by  the  absence  of 
any  wave  at  the  time  of  the  arrow  in  the  intercalated  diagram  of  Fig.  101 


Fig.   101.    Shows  a  nodal  extra-systole  (a'  and  r'),  the  auricular  and  ventricular  systoles 
as  shown  in  the  diagram  are  premature  and  simultaneous. 


during  the  irregular  period,  which  is  the  time  when  it  was  due.  Here  then 
we  have  evidence  that  both  auricle  and  ventricle  contracted  prematurely 
and  simultaneously.  In  the  ventricular  and  auricular  forms  no  difficulty 
is  found  in  recognizing  that  the  extra-stimulation  must  have  affected  either 
one  chamber  or  the  other,  but  in  this  form  we  have  to  consider  where  a  stimu- 


FiG.  102.     Shows  two  nodal  extra-systoles  (a'),  the  auricular  waves  a   appearing  prema- 
turely and  at  the  same  time  as  the  extra-systole  in  the  radial. 

lation  could  arise  that  would  at  once  affect  both  chambers.  If  all  the  possi- 
bilities be  considered,  we  are  driven  by  a  process  of  exclusion  to  attribute 
the  source  of  this  stimulation  to  the  tissue  that  joins  auricle  and  ventricle, 
and  almost  to  a  certainty  to  that  portion  described  as  the  auriculo-ventri- 
cular  node  (2,  Fig.  2).  This  will  be  brought  out  more  clearly  in  the  later 
discussion. 


THE  EXTRA-SYSTOLE  159 

In  many  cases  it  is  difficult  to  tell  whether  the  stimulus  producing  the 
extra-systole  arises  in  the  ventricle  at  the  same  time  as  the  normal  auricular 
systole,  or  whether  they  have  contracted  together  in  response  to  an  abnormal 
stimulation.  In  the  latter  case  the  abnormal  stimulation  affects  the  auricle 
at  the  same  time  that  the  normal  was  due,  so  that  we  do  not  get  the  proof 
of  the  premature  contraction  of  the  auricle.  My  reason  for  this  suggestion 
is  that  sometimes  we  meet  with  a  variety  of  extra-systoles  in  the  same 
patient,  indicating  that  at  one  time  the  auricle  is  prematurely  stimulated, 
at  another  time  the  ventricle,  and  again  both  ventricle  and  auricle  together. 
This  is  well  seen  in  Fig.  103,  Plate  II,  where  three  forms  of  extra-systole 
occur.  The  wave  a'  in  the  irregular  period  C  is  manifestly  an  auricular  extra- 
systole  followed  by  a  premature  carotid  wave  c',  which  corresponds  in  time 
to  the  extra-systole  in  the  radial  tracing.     In  the  irregular  period  B,  the 


Fig.  105.  Shows  two  nodal  extra-systoles.  Diuing  the  irregular  period  A,  the  large 
auricular  wave  a'  appears  at  the  normal  auricular  period,  while  during  the  irregular  period  B, 
a'  and  r'  occur  prematurely  and  synchronously. 


auricular  wave  a'  appears  at  its  normal  interval,  but  in  the  radial  tracing  there 
is  seen  an  extra-systole  which  appears  at  the  same  time  as  the  wave  a' .  This 
is  undoubtedly  a  ventricular  extra-systole.  In  the  irregular  periods  A  and  D, 
the  conditions  are  not  the  same.  The  wave  a'  here  has  quite  a  different 
appearance  from  that  in  either  B  or  C,  being  broader  at  the  top.  It  is 
difficult  to  be  certain  whether  it  appears  before  the  normal  auricular  systole 
was  due,  as  there  is  a  little  sinus  arrhythmia — the  pulse  periods  not  being  of 
equal  duration.  The  absence  of  the  extra-systole  in  the  radial  does  not 
imply  that  the  left  ventricle  did  not  contract,  for,  as  we  shall  see  later,  the 
ventricle  may  contract  so  feebly  that  a  pulse-wave  does  not  reach  the  wrist. 
That  they  are  probably  nodal  extra-systoles  can  be  inferred  from  the  nature 
of  the  extra-systoles  that  occurred  from  time  to  time  in  the  patient.  Thus  the 
typical  auricular  extra-systole  in  Fig.  99  is  from  the  same  patient.  Fig.  104, 
Plate  II,  is  also  from  the  same  patient,  and  shows  two  irregular  periods  in 
which  the  large  wave  a'  appears  before  a  normal  auricular  systole  is  due. 


160  DISEASES  OF  THE  HEART 

From  this  I  suggest  that  this  wave  is  of  the  same  nature  as  that  of  a'  in  the 
irregular  periods  A  and  D,  Fig.  103,  Plate  II,  namely,  due  to  a  premature 
and  simultaneous  contraction  of  auricle  and  ventricle.  The  suggestion  that 
the  abnormal  stimulation  may  afifect  auricle  and  ventricle  at  the  time  the 
normal  auricular  stimulus  is  due  is  supported  by  such  a  tracing  as  Fig.  105. 
There  are  here  two  irregular  periods,  A  and  B,  due  to  extra-systoles.  The 
extra-systole  in  A  is  only  slightly  premature,  and  the  large  wave  a'  appears 
at  the  time  the  normal  auricular  wave  was  due.  The  extra-systole  in  B 
appears  earlier,  with  the  result  that  the  large  wave  a'  appears  before  the 
time  the  normal  auricular  systole  was  due,  so  tha?t  here  auricle  and  ventricle 
contracted  simultaneously  and  prematurely. 

This  explanation  of  the  occurrence  of  the  extra-systole  arising  in  the 
auriculo-ventricular  node  is  not  the  one  usually  accepted.  It  has  been 
assumed  that  these  cases  are  really  ventricular  extra-systoles,  and  that  the 
stimulus  has  passed  back  and  prematurely  stimulated  the  auricle,  '  a  retro- 
grade extra-systole  '  as  it  has  been  called.  But  that  this  explanation  is 
not  tenable  can  be  proved  on  several  grounds.  As  was  shown  in  Figs.  89,  90 
Plate  II,  91  Plate  II,  and  92,  there  is  no  tendency  for  the  stimulation 
from  the  ventricular  extra-systole  to  afifect  the  auricular  rhythm.  If  the 
stimulus  does  travel  back,  the  rate  backward  must  be  much  greater  than 
that  at  which  the  normal  stimulus  travels  forward,  for  as  shown  in  the 
diagram,  in  Fig.  101,  the  time  of  the  ventricular  systole  is  exactly  at  the 
same  time  as  the  auricular.  That  this  time  should  be  shorter  is  very  unlikely 
for  two  reasons — (1)  the  auriculo-ventricular  bundle  would  be  stimulated 
by  the  ventricular  extra-systole  so  soon  after  its  conductivity  had  been 
exercised,  that  it  would  not  have  recovered,  and  a  backward  stimulus  would 
therefore  be  delayed,  just  as  the  normal  stimulus  was  delayed  after  the 
extra-systole  in  Fig.  89.  (2)  The  simultaneous  and  premature  contraction 
occurs  in  patients  in  whom  the  conductivity  of  the  auriculo-ventricular 
bundle  is  impaired,  as  I  shall  show  presently. 

§  147.  The  condition  of  the  a.-v.  bundle  in  cases  showing  extra- 
systoles — From  what  I  have  said,  there  are  three  forms  of  extra-systole 
all  arising  demonstrably  from  different  places  in  the  heart.  Moreover, 
certain  individuals  exhibit  all  these  forms,  and  it  is  therefore  reasonable 
to  infer  that  all  these  are  due  to  some  common  cause.  When  all  the  possi- 
biUties  are  considered,  the  suggestion  that  the  primitive  tissue  is  the  seat 
is  the  most  plausible,  and  the  question  then  arises,  is  there  any  further 
evidence  to  be  elicited  as  to  the  condition  of  this  primitive  tissue  ? 

The  only  clinical  evidence  of  the  condition  of  the  primitive  tissue  is  to 
be  found  in  measuring  the  rate  at  which  the  stimulus  for  contraction  passes 


THE  EXTRA-SYSTOLE  161 

along  the  a. -v.  bundle  from  auricle  to  ventricle.  This  rate  is  found  by  measur- 
ing in  jugular  tracings  the  time  between  the  beginning  of  the  auricular  wave 
and  the  beginning  of  the  carotid  wave — the  a-c  interval  (between  lines 
1  and  3  in  the  tracings  of  the  jugular  pulse  as  in  Figs.  47  and  48),  as  I  have 
called  it.  This  interval  is  occupied  by  three  events  :  (1)  the  systole  of  the 
auricle  ;  (2)  the  transmission  of  the  stimulus  from  auricle  to  ventricle  ;  (3)  a 
minute  portion  of  time  taken  up  by  the  interval  during  which  the  ventricular 
pressure  is  rising  before  the  opening  of  the  aortic  valves.  As  (3)  is  practically 
constant,  any  variation  in  the  duration  of  the  a-c  interval  can  be  attributed 
to  a  variation  in  the  rate  of  the  stimulus  conduction  in  the  a. -v.  bundle 
(see  §  163).  In  normal  individuals,  this  period  very  rarely  exceeds  one-fifth 
of  a  second.  In  hearts  acting  too  frequently,  this  interval  is  usually  less, 
sometimes  one-tenth.  One  may  suspect  something  wrong  with  the  a.-v. 
bundle  when  this  period  is  one-fifth  of  a  second  when  the  heart  is  beating 
rapidly,  for  the  stimulus  that  quickens  the  heart-rate  will  also  quicken  the  rate 
of  conduction  when  the  a.-v.  bundle  is  intact.  In  healthy  slow-acting 
hearts,  in  which  there  is  a  variation  in  the  heart's  rate,  it  is  found  that  whether 
the  heart's  pauses  are  short  or  long,  the  a-c  interval  preserves  a  remarkable 
constancy.  The  best  instance  of  this  is  found  in  the  young,  and  in  those 
healthy  adults  in  whom  there  is  present  the  sinus  form  of  irregularity.  Thus 
in  Fig.  79,  p.  146,  the  long  pause  is  due  to  a  standstill  of  the  whole  heart, 
and  is  a  very  typical  example  of  '  sinus  irregularity  ',  probably  of  vagal 
origin,  and  here  the  constancy  of  the  a-c  interval  (spaces  A)  is  very  well  seen. 

On  the  other  hand,  if  we  look  at  the  interval  between  the  auricular  extra- 
systole  a'  and  the  following  carotid  wave  c'  in  Figs.  98  and  99,  we  find  it 
markedly  increased.  This  implies  that  the  conductivity  in  the  a.-v.  bundle 
had  not  recovered  from  its  previous  stimulation,  and  the  slowness  of  recovery 
is  the  proof  of  inefficiency.  In  cases  of  ventricular  extra-systole,  as  in 
Figs.  89,  90  Plate  II,  and  91  Plate  II,  and  in  cases  of  extra-systole  arising 
at  the  a.-v.  node,  as  in  Fig.  101,  we  find  frequently  a  distinct  shortening  of 
the  a-c  interval  after  a  long  period  of  rest,  and  a  lengthening  when  the  period 
of  rest  is  short.  This  is  well  illustrated  in  Fig.  106,  Plate  II,  where  after  the 
long  pause  the  a-c  interval  becomes  less  than  one-fifth  of  a  second  {A^), 
but  with  each  succeeding  beat  it  gradually  lengthens  (.^^  Ar^  A^)  until  it 
exceeds  one-fifth  of  a  second  in  duration.  In  elderly  people  in  whom  extra- 
systoles  occur,  this  variation  in  the  conductivity  of  the  a.-v.  bundle  is  almost 
always  present.  I  have  also  met  with  an  increase  of  the  a-c  interval,  and 
extra-systoles  after  rheumatic  fever. 

§  148.  The  dropping  out  of  the  beat  after  the  extra-systole. — In 
most  instances  there  is  a  long  pause  after  the  extra-systole — the  so-called 

MACKENZIE  J^J 


162  DISEASES  OF  THE  HEART 

compensatory  pause  (pulse  intermission).  The  reason  given  by  Engelmann, 
and  usually  accepted,  is  that  the  ventricle  is  so  exhausted  after  the  preceding 
contraction  that  it  is  refractory  to  the  following  normal  stimulus.  While  this 
may  be  the  explanation  when  the  extra-systole  is  produced  experimentally, 
it  does  not  hold  good  for  the  spontaneous  extra-systole  in  man.  In  Figs.  89, 
p.  152,  and  90  Plate  II,  and  in  the  irregular  period -B  of  Fig.  91,  Plate  II,  there 
is  no  compensatory  pause,  because,  as  can  be  seen  from  the  intercalated 
diagrams  in  Figs.  89,  and  91  Plate  II,  the  stimulus  from  the  auricular 
contraction  immediately  following  the  extra-systole  did  get  through  and 
stimulated  the  ventricle.  In  each  case,  however,  the  stimulus  took  a  much 
longer  time  to  pass  from  auricle  to  ventricle.  Ih  Fig.  91,  Plate  II,  the 
stimulus  failed  to  get  through  during  the  irregular  period  C,  for  there  is  no 
ventricular  response  to  the  auricular  contraction  after  the  extra-systole.  In 
these  and  in  many  similar  instances,  it  is  manifest  that  the  reason  the  ventricle 
does  not  contract  in  response  to  the  stimulus  from  the  auricle  after  an  extra- 
systole,  is  that  the  stimulus  is  blocked  in  its  passage  over  the  a.-v.  bundle. 
Hewlett  202  lias  recently  recorded  a  case  in  which  the  ventricle  did  not  respond 
to  the  stimulus  from  an  auricular  extra-systole,  and  the  same  explanation 
is  given  by  him.  From  the  foregoing  considerations,  I  make  the  suggestion 
that  the  compensatory  pause  is  not  due  to  the  ventricle  being  refractory, 
but  to  the  a.-v.  bundle  being  refractory  and  not  conveying  the  stimulus  to 
the  ventricle,  which  therefore  stands  still  tiU  the  next  physiological  stimulus 
comes  down  from  the  auricle. 

§  149.  Reasons    for  attributing    the   origin   of    extra-systoles  to 

affection   of   the   remains   of   the   primitive    cardiac   tube (i)  An 

a  priori  reason,  in  the  fact  that  the  primitive  tube  possesses  a  greater 
excitabiHty  than  the  auricular  and  ventricular  tissue,  and  that  therefore 
an  abnormal  stimulus  is  more  likely  to  arise  in  this  tissue. 

(2)  It  satisfactorily  accounts  for  the  three  forms  of  extra-systole,  especi- 
ally when  in  any  individual  two  or  more  forms  arise.  It  seems  more 
reasonable  to  assume  that  the  one  organ  or  tissue  being  degenerated  gives 
rise  to  an  extra  stimulus,  now  at  the  auricular  portion,  now  at  the  ventricular 
portion  of  the  bundle,  and  now  at  the  a.-v.  node,  than  to  say  it  arises  now 
in  the  auricle,  and  now  at  the  ventricle,  and  again  at  some  other  part  of  the 
ventricle  which  propagates  a  stimulus  back  to  the  auricle. 

(3)  The  frequent  association  of  extra-systole  with  impaired  conductivity 
of  the  a.-v.  bundle  impHes  an  affection  of  the  tissue  in  question.  It  may  be 
objected  that  an  extra-systole  is  an  evidence  of  exalted  function,  while 
impaired  conductivity  is  an  evidence  of  depressed  function.  GaskeU  has 
shown  that  the  rate  at  which  a  stimulus  passes   across  a  bridge  of   heart 


THE  EXTRA-SYSTOLE  163 

muscle  can  be  retarded  by  narrowing  the  bridge  over  which  the  stimulus 
for  contraction  has  to  pass.  In  the  cases  of  associated  depressed  conduc- 
tivity and  extra-systole,  there  is  destruction  of  some  part  of  the  bundle, 
while  the  degenerative  process  which  does  this,  renders  the  part  more 
irritable,  and  we  meet  with  the  combination  of  extra-systoles  and  heart-block. 

(4)  These  degenerative  processes  are  more  common  in  advanced  years, 
hence  it  is  in  the  elderly  we  find  extra-systole  most  frequent.  So  far  as 
Dr.  Keith  has  examined  the  hearts  of  patients  I  have  sent  him  who  showed 
extra-systoles  during  life,  he  has  invariably  found  evidence  of  degeneration  of 
the  a.-v.  node  and  bundle.  As,  however,  there  was  always  present  degene- 
ration of  the  coronary  artery  and  muscular  fibres  of  the  ventricle,  it  does 
not  exclude  the  possibility  of  ventricular  degeneration  giving  rise  to  the 
extra-stimulus,  except  for  the  a  priori  reason  already  given. 

I  give  these  reasons,  not  that  I  consider  they  are  conclusive,  but  as 
suggesting  a  possible  explanation.  The  matter,  however,  awaits  further 
experimental  work  before  it  can  be  finally  settled.  The  explanation  given 
seems  to  me  to  be  more  satisfactory  than  the  one  hitherto  adopted. 

§  150.  Conditions    inducing    extra-systoles A  condition  necessary 

to  the  production  of  an  extra-systole  is  an  undue  excitabihty  of  the  remains 
of  the  primitive  cardiac  tube.  It  is  not  easy  in  all  cases  to  understand 
how  this  arises.  In  elderly  people  there  are  almost  invariably  sclerotic 
changes  in  the  coronary  artery,  and  especially  in  the  branch  that  supphes 
the  a.-v.  node  and  bundle  ;  and  secondary  changes  are  usually  present 
in  these  structures.  I  have  reasoned,  therefore,  that  these  secondary 
changes  increase  the  excitability  of  this  tissue,  so  that  the  stimulus  for 
contraction  arises  quicker  here  than  at  the  sinus.  A  great  many  facts 
point  to  the  reasonableness  of  this  interpretation.  A  normal  slow  sinus 
rhythm  gives  an  opportunity  for  the  stimulus  to  arise  elsewhere,  and  it 
is  in  the  elderly  with  a  slow  pulse  that  one  most  often  finds  extra-systoles. 
On  the  other  hand,  extra-systoles  sometimes  occur  in  rapidly-beating 
hearts,  perhaps  because,  although  the  sinus  is  discharging  impulses  more 
rapidly  than  normal,  these  are  not  sufficient  to  exhaust  the  irritability  of 
some  very  sensitive  point  in  the  primitive  tube.  But  not  infrequently 
when  a  heart  which  ordinarily  exhibits  extra-systoles  is  accelerated,  as  in 
slight  fever,  the  extra-systoles  disappear,  because  the  impulses  arising  from 
the  sinus  are  now  sufficient  to  exhaust  the  irritability  of  the  part  which 
ordinarily  gives  rise  to  the  extra-systole. 

Another  condition  that  tends  to  increase  the  excitability  of  this  structure 
is  the  changes  subsequent  to  rheumatic  affections  of  the  heart,  for  in  these 
cases  extra-systoles  are  often  present,  and  frequently  the  heart's  contraction 

m2 


164  DISEASES  OF  THE  HEART 

starts  from  the  a. -v.  node  continuously.  Digitalis  may  give  rise  to  them 
in  rheumatic  hearts.  Dyspeptic  and  neurotic  people  are  often  liable.  That 
other  conditions  give  rise  to  extra-systoles  is  also  evident  from  the  fact 
that  they  may  occur  in  young  people  in  whom  there  is  no  rheumatic  history 
and  no  cardio-sclerosis,  and  whose  after-history  reveals  no  sign  of  heart 
trouble. 

§  151.  Sensations  produced  by  extra-systoles — Some  patients  are 
conscious  of  a  quiet  transient  fluttering  in  the  chest  when  an  extra- 
systole  occurs ;  others  are  aware  of  the  long  pause  *  as  if  their  heart  had 
stopped '  ;  while  others  are  conscious  of  the  big  beat  that  frequently 
follows  the  long  pause.  So  violent  is  the  effect  of  this  after-beat  that 
in  neurotic  persons  it  may  cause  a  shock  followed  by  a  sense  of  great 
exhaustion.  Most  patients  are  unconscious  of  the  irregularity  due  to 
the  extra-systole  until  their  attention  is  called  to  it  by  the  medical 
attendant.  Both  being  ignorant  of  its  origin,  and  it  being  characteristic 
of  human  nature  to  associate  the  unknown  with  evil,  patient  and  doctor 
are  too  often  unnecessarily  alarmed. 

§  152.  Prognosis — The  most  serious  thing  about  these  cases  is  that 
the  consciousness  of  having  an  irregularity  sometimes  makes  a  patient 
introspective  and  depressed.  He  keeps  feeling  his  pulse,  and  communicates 
his  doleful  tale  whenever  he  finds  a  sympathetic  ear. 

As  the  process  which  gives  rise  to  it  in  elderly  people  is  the  same  as 
that  which  produces  the  tortuous  temporal  arteries,  no  more  significance 
should  be  attached  to  the  one  symptom  than  to  the  other.  I  have  followed 
cases  for  many  years,  and  watched  them  pass  through  seasons  of  sickness 
and  of  stress,  and  have  seen  no  reason  to  attach  any  serious  import  to  this 
symptom.  In  rare  instances,  the  heart,  from  being  occasionally  irregular, 
has  after  many  years  become  continuously  irregular  for  short  or  long  periods, 
and  in  a  few  the  permanent  establishment  of  the  nodal  rhythm  has  been  the 
means  of  hastening  the  end.  But  this  is  infrequent,  and  in  cases  of  cardio- 
sclerosis has  only  happened  in  advanced  life,  and  the  patient  should  on  no 
account  be  frightened  by  being  warned  of  the  possible  occurrence  of  this 
unlikely  contingency.  In  younger  and  neurotic  people  I  have  never  seen 
it  lead  to  any  bad  results.  It  may  appear  in  serious  affections  of  the  heart, 
as  in  febrile  complaints,  but  it  does  not  of  itself  add  to  the  gravity  of  the 
condition,  though  I  am  not  sure  that  when  due  to  an  acute  affection  of  the 
heart,  as  in  pneumonia  and  rheumatic  fever,  it  may  not  be  a  sign  of  invasion 
of  the  myocardium  by  the  diseased  process. 

§  153'  Treatment. — If  the  patient  is  aware  of  the  irregularity  he 
should  be  assured  that  there  is  no  cause  for  alarm.     It  is  useless  to  attempt 


THE  EXTRA-SYSTOLE  165 

to  treat  the  irregularity  itself.  If  in  other  respects  the  patient  is  well,  then 
there  is  no  need  for  any  special  treatment.  If  the  patient  be  suffering 
from  conditions  which  seem  to  promote  the  irregularity,  such  as  worry, 
fatigue,  dyspepsia,  the  treatment  should  be  devoted  to  the  removal  of  the 
pre-disposing  cause.  In  people  with  temporary  high  blood-pressure  who 
show  extra-systoles,  I  find  plenty  of  healthy  exercise  in  the  open  air  specially 
beneficial,  though  until  they  get  trained,  the  extra-systoles  may  at  times 
become  more  frequent  by  the  exertion. 


CHAPTER   XX 

The    Nodal    Rhythm    (Continuous    Irregularity    of    the    Heart — 

Paroxysmal  Tachycardia) 

§  154.  Meaning  of  the  term  '  nodal  rhythm  '. 

155.  Etiology. 

156.  Manner  in  which  the  nodal  rhythm  leads  to  heart  failm-e. 

157.  Classification. 

158.  Cases  in  which  the  rate  is  not  markedly  increased.     Symptoms.     Prognosis.     Treat- 

ment. 

159.  Cases  in  which  the  rate  is  greatly  increased.     Symptoms.     Prognosis.     Treatment. 

160.  Cases  in  which  the  nodal  rhythm  is  transient  and  recurrent  (paroxysmal  tachycardia). 

Symptoms.     Prognosis.     Treatment. 

§  154.  Meaning  of  the  term  *  nodal  rhythm  ' The  term  '  nodal 

rhythm  '  is  apphed  to  that  action  of  the  heart  where  the  auricles  and  ven- 
tricles contract  simultaneously — the  ventricular  contraction  preceding  the 
auricular  by  about  one-tenth  of  a  second  in  the  great  majority  of  cases. 
Prom  this  fact,  proved  by  experimental  as  well  as  clinical  evidence  (§  115), 
it  is  reasoned  that  the  starting-place  is  no  longer  at  the  remains  of  the  sinus, 
but  in  the  remains  of  the  primitive  cardiac  tube  lower  down.  It  has  been 
established  that  when  the  a.-v.  bundle  has  been  cut  across  after  it  has  left 
the  a.-v.  node  (Fig.  2),  the  auricle  and  ventricle  beat  at  independent  rates — 
the  ventricular  rate  being  slow  (true  ventricular  rhythm,  §  168).  In  the 
vast  majority  of  cases  of  nodal  rhythm  the  heart  beats  more  rapidly  than 
normal,  and  the  auricle  and  ventricle  contract  together.  Prom  these 
circumstances  I  have  reasoned  that  here,  as  in  the  case  of  the  nodal  extra- 
systole,  the  source  of  the  heart's  contraction  starts  at  or  about  the  a.-v. 
node — hence  the  term  '  nodal  rhythm  '.  Whether  this  may  ultimately  be 
found  to  be  the  real  starting-point  or  not,  the  cases  described  under  this 
term  have  such  well-marked  characters  that  it  is  imperative  that  they 
should  be  singled  out  for  special  recognition.  The  nodal  rhythm  is  present 
in  the  majority  of  cases  of  severe  heart  failure,  and  in  a  great  many  the 
immediate  breakdown  is  directly  attributable  to  the  inception  by  the  heart  of 
this  abnormal  rhythm.  When  it  occurs  the  heart  is  at  once  placed  at 
a  great  disadvantage  in  carrying  on  its  work,  and  the  extent  of  the  impair- 
ment of  the  circulation  depends  on  the  integrity  of  the  heart  muscle. 


THE  NODAL  RHYTHM 


167 


I  have  already  drawn  attention  to  the  outstanding  features  of  these 
cases,  where  it  was  shown  that  the  ventricular  venous  pulse  indicated 
a  change  in  the  starting-place  of  the  heart's  contraction,  and  that  all  sign 
of  the  auricular  contraction  at  the  normal  period  of  the  cardiac  cycle  dis- 


B^^^^^^^^^^^^^^^Hj^^^^^^^^B 

lffl||n|^^H||^|H|^^M^ 

Fig.  107.     Tracing  of  the  radial  pulse  showing  the  irregularity  characteristic  of  the  sudden 

inception  of  the  nodal  rhythm, 

appeared.     Detailed  proof  of  this  is  given  in  the  record  of  illustrative  cases 
cited  in  Appendix  II. 

The  most  obvious  sign  which,  in  the  great  majority  of  cases,  indicates 
this  abnormal  rhythm,  is  the  character  of  the  heart's  action.     Except  in 


Fig.  108.     Shows  a  type  of  irregular  pulse  with  the  nodal  rhythm. 

some  cases  of  excessive  rapidity,  this  rhythm  is  invariably  irregular  ;  the 
irregularity  sometimes  being  extreme.  It  may  be  occasionally  so  slight 
that  it  is  apt  to  be  overlooked,  but  if  the  heart's  action  be  watched  for  a  few 
minutes,  it  will  show  variation  in  rhythm.     The  character  of  the  irregularity 


Fig.  109.     Characteristic  type  of  nodal  irregularity  occurring  in  the  elderly. 

will  be  better  realized  by  looking  at  such  tracings  as  Figs.  107,  108,  109,  and 
110,  where  the  rhythm  will  be  seen  to  be  nondescript  and  disorderly  (other 
examples  will  be  found  in  §  115,  and  in  Appendix  II). 

§  155.  Etiology. — The  exact  pathological  details  of  these  cases  have  not 
been  sufficiently  worked  out,  but  from  an  examination  of  a  series  of  hearts 
in  which    I  was  able  to  demonstrate  all  the  features  of  this  irregularity 


168 


DISEASES  OF  THE  HEART 


during  life,  Dr.  Keith  has  found  evidence  of  pathological  changes  which, 
with  the  well-authenticated  clinical  evidence,  permits  the  following  pro- 
visional descriptive  account  : — 

The  great  majority  of  cases  of  nodal  rhythm  are  found  among 
those  who  have  suffered  from  rheumatic  affection  of  the  heart,  or  cardio- 
sclerosis. In  rheumatic  hearts  there  are  often  deposits  of  cells  scattered 
through  the  heart,  which  ultimately  cicatrize.  These  deposits  when  on  or 
near  the  a. -v.  bundle  impair  its  function,  and  this  is  frequently  recognized 
in  early  cases  by  the  delay  which  occurs  between  the  contraction  of  the 
auricle  and  ventricle,  from  the  retarded  transmission  of  the  impulse  through 
the  connecting  fibres.  A  later  result  may  be  obtained  when  the  cicatri- 
zation irritates  the  bundle,  and  renders  it  more  excitable  than  the  sinus. 
In  accordance  with  the  law  that  the  contraction  starts  at  the  most  excitable 
part  of  the  primitive  tissue,  the  contraction  of  the  heart  then  originates 
in  this  more  irritable  part.     Somewhat  analogous  changes  follow  in  cardio- 


Apex  beat 


Radial  pulse 


HMJM^Vn^/^, 


Fig.  110.    Simultaneous  tracings  of  the  apex  beat  and  of  the  radial  pulse,  showing  charac- 
teristic type  of  nodal  irregularity  during  a  period  of  severe  heart  failure. 

sclerosis  and  in  degeneration  of  the  coronary  arteries.  In  certain  typical 
cases  of  this  irregularity  Keith  has  found  the  artery  supplying  the  bundle 
affected  with  marked  arterio-sclerosis,  and  with  an  invasion  of  fibrous  tissue 
in  and  around  the  a. -v.  node  and  bundle  (see  report  of  cases  in  Appendix  II). 

In  these  cases  the  increased  irritability  of  the  degenerated  a. -v.  node  and 
bundle  seem  to  lead  to  the  inception  of  the  abnormal  rhythm.  Another 
cause  of  nodal  rhythm  is  suggested  by  some  cases  in  which  there  has 
been  found  such  distension  of  the  auricle  that  it  appeared  impossible  that 
the  stimulus  from  the  sinus  could  have  been  transmitted  through  the 
attenuated  muscle  (see  pathological  report  of  Case  8  in  Appendix  II).  In 
my  earlier  investigations  it  seemed  to  me  that  the  auricle  must  have  been 
paralysed  during  life,  particularly  as  in  these  cases  no  evidence  was  afforded 
of  the  auricular  contraction. 

§  156.  Manner  in  which  the  nodal  rhythm  leads  to  heart  failure. 
— Mc William  129  has  demonstrated  experimentally  that  when  a  heart  is 
made  to  reverse  its  contraction,  the  ventricle  contracting  first,  there  is 
at  once  a  great  embarrassment  of  the  circulation.  It  is  readily  intelligible 
that  the  heart  being  adapted  to  perform  its  work  most  efficiently  in  such 


THE  NODAL  RHYTHM  169 

a  manner  that  the  auricles  contract  and  then  the  ventricles,  reversal  of 
this  sequence  must  be  against  efficiency.  When,  therefore,  the  ventricle 
starts  the  contraction  the  heart  is  at  once  embarrassed  in  its  work.  This 
embarrassment  is  made  evident  by  a  diminution  in  the  reserve  force,  and  the 
symptoms  produced  are  simply  those  that  imply  an  exhaustion  of  this 
reserve  force. 

The  degree  to  which  the  heart  failure  may  proceed  depends  on  the 
integrity  of  the  heart  muscle.  If  this  be  good,  then  it  is  able  to  cope 
with  the  embarrassment  induced  by  the  abnormal  rhythm,  and  very  little 
change  may  take  place.  If  it  be  much  degenerated,  and  particularly  if  the 
inception  of  the  rhythm  is  accompanied  by  excessive  rapidity  and  dilatation 
of  the  heart,  then  the  condition  becomes  speedily  very  grave. 

§  157*  Classification. — In  the  analysis  of  over  600  cases  where  this 
abnormal  rhythm  has  occurred,  I  have  sought  for  the  facts  that  would 
be  of  use  in  treatment.  With  our  imperfect  knowledge  of  the  cause  of  this 
rhythm,  it  is  not  yet  possible  to  give  a  scientific  analysis,  and  I  therefore 
present  the  matter  in  the  following  classification,  which  will  be  found  to  be 
one  readily  applied  and  very  useful  in  practice.  As  the  manner  in  which 
the  heart  carries  on  its  work  after  the  inception  of  the  nodal  rhythm  depends 
a  great  deal  upon  the  rate  of  its  contraction,  the  cases  can  be  classified  as 
follows  : — 

(a)  Where  the  rate  is  not  markedly  increased. 

(6)  Where  the  rate  is  greatly  increased. 

(c)  Where  the  nodal  rhythm  is  transient  and  recurrent  (one  form  of 

paroxysmal  tachycardia). 

(d)  Where  the  rate  is  markedly  slower  than  normal  (nodal  bradycardia, 

see  p.  337). 

§  158.  Cases  in  which  the  rate  is  not  markedly  increased. 
Symptoms. — In  a  great  many  people  this  continued  irregular  action  of  the 
heart  is  found  with  the  rate  about  normal  or  very  slightly  increased  (under  90). 
The  change  in  the  heart's  action  may  take  place  so  quietly  that  the  patient 
may  be  unconscious  of  it,  and  continue  at  his  work,  which  may  be  laborious. 
Usually  there  is  a  slight  limitation  of  the  field  of  cardiac  response,  and 
many  go  about  quietly  for  years  with  little  further  trouble,  even  though 
the  legs  may  become  a  little  swollen.  Sooner  or  later  this  tendency  to 
oedema  increases,  yielding  at  first  to  treatment  but  tending  to  recur,  until 
finally  extreme  heart  failure  sets  in.  This  form  in  rheumatic  hearts  may 
occur  in  early  life  ;  in  cardio-sclerosis,  rarely  before  fifty,  becoming  more 
frequent  with  increasing  years. 

Prognosis. — Many    people    may    show    this    characteristic    irregularity 


170  DISEASES  OF  THE  HEART 

and  be  engaged  in  arduous  labour  for  many  years.  In  such  cases  if  it 
occurs  before  fifty  years  of  age,  there  is  usually  a  past  history  of  rheumatic 
fever.  When  it  occurs  in  later  life,  the  extent  to  which  the  field  of  response 
becomes  Hmited  is  the  best  guide.  If  the  field  be  fairly  good  patients  may 
go  on  quietly  for  many  years,  some  living  well  over  seventy. 

Treatment. — Unless  there  is  a  distinct  evidence  of  heart  failure,  no 
treatment  is  necessary.  If  the  heart-rate  begins  to  increase  in  frequency 
and  dropsy  sets  in,  then  the  treatment  should  follow  the  lines  laid  down 
in  the  chapters  on  treatment. 

§  159.  Where  the  rate  is  greatly  increased.  Symptoms. — The 
sensation  felt  by  the  patient  when  this  rhythm  is  first  started  may  be  so 
slight  as  to  pass  unnoticed.  Usually  he  is  conscious  of' a  curious  fluttering 
sensation  inside  the  left  chest.  This  sensation  is  very  characteristic  and 
almost  pathognomonic.  It  may  be  described  variously  according  to  the 
literary  gift  of  the  sufferer,  but  the  essential  feature  is  the  soft  and  gentle 
movements,  not  rhythmical,  but  varying  softly  in  intensity,  in  striking 
contrast  to  the  sensations  that  may  arise  from  stimulation  of  the  heart 
during  a  normal  rhythm,  as  in  palpitation.  Frequently  this  sensation  is 
so  disquieting  that  the  patient  rests,  or  walks  about  cautiously  and  quietly. 
About  the  same  time  the  patient  remarks  a  distinct  hmitation  in  the  field 
of  cardiac  response,  the  exertion  that  he  was  wont  to  undertake  with  comfort 
now  inducing  breathlessness. 

The  associated  heart  failure  may  be  so  extreme  that  in  a  few  days,  or 
even  in  a  few  hours,  evidences  of  imminent  peril  are  shown.  The  patient 
has  to  keep  in  bed,  the  dyspnoea  being  so  great  that  he  cannot  lie  on  his 
back,  but_^must  be  propped  up.  If  the  patient  survives,  oedema  of  the  legs 
quickly  supervenes,  the  hps  become  livid  and  the  face  swollen.  The  pulse  is 
small,  rapid,  and  usually  irregular,  the  beats  varying  remarkably  in  strength. 
The  character  of  the  heart's  action  at  this  stage  can  be  reahzed  from  such 
tracings  as  Figs.  107,  p.  167,  and  110,  p.  168.  The  veins  of  the  neck  are 
often  fuU  and  pulsate  with  great  rapidity.  The  heart  dilates  in  a  few  hours, 
sometimes  extending  two  inches  in  the  transverse  direction.  The  sounds 
alter,  becoming  short  and  sharp,  and  if  the  heart's  action  is  rapid,  often 
no  murmur  may  be  detected.  If  there  has  previously  been  a  pre-systolic 
mitral  murmur,  it  disappears,  and  if  the  heart's  action  is  fairly  slow  a  dia- 
stolic mitral  murmur  may  be  detected,  but  never  a  pre-systohc.  The  liver 
becomes  enlarged,  and  may  be  found  pulsating  two  or  three  inches  below 
the  ribs.  The  tissues  covering  the  heart  and  the  liver  often  become 
extremely^tender  on  pressure. 

If  the  heart  does  not  slow  down  after  this  sudden  inception  of  the 


THE  NODAL  RHYTHM  171 

nodal  rhythm,  the  patient  drifts  on  to  death,  and  many  cases  of  rapid 
and  fatal  breakdown,  particularly  in  old  people,  are  directly  due  to  the 
inception  by  the  heart  of  this  rhythm  (Cases  11,  12,  and  15,  Appendix  II). 
Usually  the  heart  does  slow  down  and  the  circulation  improves,  and  the 
patient  may  so  far  recover  as  to  be  able  to  go  about  for  years  with  more  or 
less  comfort,  but  is  always  liable  to  relapses  more  or  less  severe.  One  often 
comes  across  people  who  have  had  a  continual  irregularity  of  the  heart's 
action  for  many  years,  and  they  have  learned  to  treat  themselves  with 
remarkable  success,  and  some  of  the  more  intelligent  can  give  the  physician 
very  important  information  as  to  the  relative  value  of  many  heart  drugs, 
as  digitalis  and  strophanthus. 

Prognosis. — The  prognosis  depends  on  how  the  heart  behaves,  and 
how  well  it  maintains  the  circulation  under  the  new  rhythm.  If  the  patient 
feels  little  or  no  distress  then  he  may  be  assured  of  many  years  of  fairly 
comfortable  life.  If  there  is  some  distress  in  breathing,  or  a  tendency  to 
'  bronchitis  '  and  swelling  of  the  legs,  he  may  still  live  for  many  years,  his 
life  chequered  by  attacks  of  heart  failure  more  or  less  severe.  If  the  condi- 
tion be  extreme  with  rapid  heart  and  much  dropsy  and  dyspnoea,  the  prog- 
nosis depends  on  how  he  reacts  to  treatment.  The  young,  or  those  with 
a  rheumatic  history,  usually  rally  from  their  breakdown,  and  may  be  for 
many  years  free  from  attacks.  The  elderly  also  rally  from  their  first  attacks, 
and  may  live  for  years  a  somewhat  crippled  existence.  But,  as  I  have 
already  indicated,  the  persistence  of  a  rapid  heart,  and  evidence  of  failure 
of  the  heart  to  maintain  the  circulation,  in  spite  of  treatment,  are  evidences 
of  a  very  serious  kind. 

Further  evidence  will  be  found  in  estimating  the  size  of  the  heart,  as 
dilatation  in  these  cases  is  always  an  indication  of  the  failure  of  tone,  and 
with  the  permanent  failure  of  tone  the  work  of  the  heart  is  further  grievously 
embarrassed  (Chapter  XXIII). 

Treatment. — It  should  be  borne  in  mind  that  the  condition  is  the 
outcome  of  a  series  of  changes  that  have  been  going  on  for  years,  and  that 
it  is  foolish  to  suppose  that  by  any  means  we  possess  we  are  able  to  remove 
the  diseased  processes  on  which  this  arrhythmia  depends. 

Attempts,  therefore,  to  '  cure  '  the  diseased  condition  are  futile.  What 
we  have  to  do  is,  not  to  waste  time  in  the  pursuit  of  a  hopeless  quest,  but  to 
make  the  best  of  an  irremediable  condition,  and  in  recognizing  this  we  are 
at  once  placed  in  a  position  to  render  real  help. 

When  the  change  in  rhythm  is  accompanied  by  little  distress,  no  treat- 
ment is  necessary.  When,  however,  there  is  evidence  of  distress,  treatment 
should  follow  in  the  main  the  principles  laid  down  in  the  chapters   on 


172  DISEASES  OF  THE  HEART 

treatment.  If  there  be  extreme  difficulty  in  breathing  and  great  restlessness, 
it  is  of  the  first  importance  that  rest  should  be  secured,  and  that  the  patient 
should  sleep.  For  this  purpose  sedatives  are  necessary,  and  they  should 
be  given  on  the  lines  laid  down  elsewhere. 

A  curious  and  instructive  reaction  to  digitaUs  will  be  found  in  these 
cases.  Most  of  those  whose  arrhythmia  is  of  rheumatic  origin  show  a  remark- 
able sensitiveness  to  digitalis,  the  heart  sometimes  responding  to  a  very 
few  doses,  and  at  the  same  time  becoming  much  slower  (see  §  251  and 
Appendix  VI).  On  the  other  hand,  in  many  cases  in  which  the  arrhythmia 
arises  secondarily  to  cardio-sclerosis,  the  digitaUs  has  no  effect  upon  the  heart. 

§  1 60.  Where  the  nodal  rhythm  is  transient  and  recurrent 
(paroxysmal  tachycardia) . — In  this  class  the  heart  suddenly  takes  on  the 
nodal  rhythm,  and  this  may  last  for  a  few  beats,  or  it  may  go  on  for 
minutes,  hours,  days,  or  weeks.  The  rate  is  usually  greatly  increased 
(200  per  minute  and  over),  and  is  then  recognized  as  '  paroxysmal  tachy- 
cardia '.  Sometimes  the  rate  is  not  markedly  increased,  and  in  rare  cases 
it  may  be  slower  than  normal  (Case  17,  Appendix  IV).  An  individual  may 
have  but  one  attack,  or  the  attacks  may  come  on  at  frequent  intervals 
in  the  course  of  ten  or  twenty  years,  or  they  may  be  of  great  frequency, 
occurring  every  few  weeks  or  days  ;  or  there  may  be  several  attacks  in  one 
day.  After  one  or  two  attacks  the  heart  may  settle  down  permanently 
with  the  nodal  rhythm. 

The  term  '  paroxysmal  tachycardia  '  has  been  used  to  describe  several 
conditions  that  present  a  superficial  resemblance,  but  are  fundamentally 
different  in  origin.  While  the  nature  of  the  rapid  action  was  unknown 
the  term  served  a  useful  purpose  ;  now  it  should  not  be  used  without  a  clear 
definition  of  what  is  meant.  Though  many  cases  with  a  normal  rhythm 
have  been  included  under  this  term,  the  most  striking  instances  described 
as  paroxysmal  tachycardia  in  literature  are  undoubtedly  due  to  the  inception 
of  an  abnormal  rhythm  ;  so  far  I  have  been  able  to  make  out  two  forms 
of  paroxysmal  tachycardia,  the  transient  nodal  rhythm  referred  to  here, 
and  an  auricular  form  described  on  p.  334. 

Symptoms. — In  extreme  cases  the  sensation  of  the  patient  and  the  asso- 
ciated heart  failure  are  exactly  those  described  in  §  159.  The  rhythm  in 
such  cases  may  be  quite  regular,  and  the  rate  may  be  over  200  beats  per 
minute.  The  changes  described  in  §  159  may  appear  in  a  few  hours.  With 
the  sudden  reversion  of  the  rhythm  to  the  normal,  the  change  in  the  patient's 
condition  is  even  more  remarkable  than  the  rapid  onset  of  the  symptoms 
of  heart  failure.  At  once  the  patient  heaves  a  sigh  of  relief,  and  in  a  very 
short  time,  within  half  an  hour,  all  abnormal  signs  in  the  lips,  face,  and 


THE  NODAL  RHYTHM  173 

enlarged  liver  disappear,  while  in  a  few  hours  the  heart  may  be  found  beating 
within  its  normal  limits. 

In  others,  the  paroxysmal  tachycardia  may  occur  for  a  day  or  two,  with 
no  marked  change  in  the  size  of  the  heart.  In  these,  the  patient  is  generally 
conscious  of  the  heart's  abnormal  action,  and  instinctively  avoids  active 
exertion,  either  keeping  in  bed  or  resting  in  a  chair,  or  walking  about  very 
quietly.  The  attack  usually  lasts  for  a  few  hours,  but  may  occasionally 
last  for  many  hours,  or  even  one  or  two  days.  At  the  end  of  this  time 
no  increase  in  the  size  of  the  heart  is  detectable,  and  there  is  no  sign  of 
dropsy  or  enlarged  liver.  This  condition  may  be  found  at  all  ages  over  ten 
years  (Appendix  II). 

Prognosis. — The  prognosis  in  these  cases  is  one  of  considerable  difficulty. 
The  symptoms  during  an  attack  may  be  so  alarming  that  the  inexperienced 
are  apt  to  look  upon  the  patient  as  hopelessly  stricken.  I  remember 
being  called  one  night  to  a  woman  eighty  years  of  age,  I  found  her  heart 
extremely  rapid  and  irregular,  her  face  swollen  and  livid,  and  she  was 
gasping  for  breath.  I  told  the  friends  the  end  was  approaching,  and,  calling 
to  see  her  next  morning,  I  found  her  walking  out  in  the  street.  After  that 
she  had  several  attacks  and  finally  died  during  one.  Other  patients  I  have 
watched  for  years,  when  the  symptoms  have  not  been  so  extreme,  sometimes 
only  giving  rise  to  a  slight  uneasiness  in  the  chest.  In  these  the  heart  has 
not  dilated,  though  the  rate  may  have  reached  nearly  200  per  minute.  Others 
have  had  but  one  attack,  and  I  have  watched  some  of  these  for  nearly  twenty 
years  and  they  have  had  no  other. 

In  some  the  change  from  being  transient  becomes  permanent,  and  here 
lies  the  danger.  If  the  extreme  form  of  heart  failure  persists  and  the 
dilatation  cannot  be  reduced,  then  the  patient  drifts  to  death  (Cases  10, 
11,  12,  and  15,  Appendix  II). 

The  prognosis  also  depends  on  the  degree  of  dilatation.  If  the  heart 
does  not  increase  in  size  and  the  attacks  are  transient,  then  on  the  whole 
the  prognosis  is  good,  though  in  many  cases  the  patient's  life  is  greatly 
crippled  because  of  the  fact  that  the  attacks  recur  in  spite  of  treatment. 
When  there  is  dilatation  with  the  accompanjdng  symptoms  of  dropsy  and 
enlarged  liver,  then  the  outlook  is  bad. 

Treatment. — Absolute  quiet  is  needed  during  the  attack — a  sugges- 
tion scarcely  necessary,  for  the  patient  usually  seeks  rest,  though  he  may 
move  about  quietly  with  little  distress.  A  great  many  suggestions  as  to 
the  arrest  of  these  attacks  may  be  found  scattered  through  medical  literature. 
As  the  attacks  are  commonly  but  transient,  some  remedy  employed  oppor- 
tunely seems  to  the  inexperienced  onlooker  to  restore  the  heart  to  its  normal 


174  DISEASES  OF  THE  HEART 

action.  Many  patients  themselves  have  a  knack  of  doing  something  that 
seems  to  change  the  rhythm.  Sometimes  attacks  can  be  stopped  by  the 
patient  simply  taking  a  series  of  deep  breaths,  by  slapping  the  chest,  by  the 
sudden  application  of  cold  water  to  the  chest.  Drugs  of  the  most  diverse 
character  have  been  cited  as  active  agents  in  stopping  attacks,  such  as 
nitro-glycerine  and  adrenahn.  In  my  early  days  I,  too,  thought  I  knew  how 
to  stop  attacks,  but  more  extended  experience  has  shown  me  that  when  they 
stopped  it  was  from  some  cause  unknown  to  me,  and  VhichVas  independent 
of  any  means  I  employed. 

When  signs  of  heart  failure  appear  the  treatment  should  follow  the 
lines  laid  down  in  the  chapters  on  treatment. 


CHAPTER   XXI 

Affections  of  the  Conducting  Functions  of  the  Primitive  Car- 
diac Tissue  (Heart-Block,  Adams-Stokes  Disease,  Ventricular 
Rhythm) 

§  161.  Definition. 

162.  Methods  of  recognizing  depression  of  conductivity. 

163.  Intersystolic  period  (the  a~c  interval). 

164.  Depression  of  conductivity  without  arrhythmia. 

165.  Influence  of  rest  upon  conductivity. 

166.  Arrhythmia  due  to  depression  of  conductivity. 

167.  Missed  beats  due  to  depression  of  conductivity. 

168.  Independent  ventricular  rhythm  due  to  heart-block. 

169.  Effect  of  the  auricular  contraction  on  the  radial  pulse. 

170.  Etiology. 

171.  Significance  of  the  milder  forms  of  depression  of  conductivity. 

172.  Symptoms. 
'  173.  Prognosis. 

174.     Treatment. 

§  i6l.  Definition. — In  the  last  two  chapters  the  irregular  action  of 
the  heart  was  ascribed  to  the  contraction  of  the  heart  starting  lower  down 
in  the  primitive  tissue  than  the  sinus.  In  this  chapter  another  important 
function  of  this  tissue  is  considered,  namely,  the  conduction  of  the  stimulus 
from  auricle  to  ventricle.  The  stimulus  for  contraction  reaches  the  ventricle 
from  the  auricle  by  passing  along  the  bridge  of  primitive  tissue  that  con- 
nects the  auricle  and  ventricle  (Fig.  2,  p.  15).  This  bridge  may  be  so 
affected  that  (1)  the  stimulus  is  delayed  ;  (2)  the  stimulus  is  at  times  pre- 
vented from  crossing  over  ;  (3)  the  stimulus  may  be  completely  blocked 
beyond  the  a.-v.  node,  and  the  ventricle  then  contracts  in  response  to 
a  stimulus  that  arises  in  the  uninjured  remains  of  the  a.-v.  bundle  (heart- 
block,  ventricular  rhythm). 

§  162.  Methods  of  recognizing  depression  of  conductivity Apart 

from  suitable  tracings,  the  clinical  evidence  is  limited  to  the  recognition  of 
the  fact  that  there  is  a  slow  radial  pulse,  or,  better,  a  slow  ventricular  rate, 
while  the  veins  in  the  neck  pulsate  more  frequently,  owing  to  the  normal 
rate  of  the  auricular  contractions  being  maintained.  If  the  ventricular 
contractions  are  over  thirty-six  per  minute,  these  may  have  a  distinct 
relationship    to  the   auricular  waves   in   the  jugular  pulse,   the   ventricle 


176  DISEASES  OF  THE  HEART 

responding  to  every  second,  third,  or  fourth  auricular  contraction.  When 
the  ventricular  contractions  are  about  thirty  or  under,  they  are  probably 
independent  of  the  auricle,  and  auricle  and  ventricle  beat  at  independent 
rates  and  in  response  to  independent  stimuli. 

When  there  is  a  mere  delay  in  the  response  of  the  ventricle  to  the  stimulus 
from  the  auricle,  the  evidence  is  very  scanty,  apart  from  graphic  records. 
I  have,  however,  in  cases  of  mitral  stenosis  been  able  to  recognize  this 
delay  by  a  slight  separation  of  the  presystolic  murmur  from  the  first  sound 
of  the  heart  (represented  diagrammatically  by  the  shading  in  Figs.  112, 
p.  177  ;  272,  p.  365,  and  265,  Plate  V).  Occasionally  '  missed  beats  '  or  pulse 
intermissions  are  due  to  the  auricular  stimulus  failing  to  provoke  a  ventri- 
cular contraction,  and  a  strong  suspicion  of  the  nature  of  this  irregularity 
may  be  aroused  by  observing  that  during  the  pause  the  ventricular 
sounds  are  absent  ;  this  distinguishes  it  from  most  cases  of  extra- 
systole,  in  which,  as  has  already  been  described,  there  are  usually 
heard  two  short,  sharp  sounds,  the  result  of  the  weak,  short,  premature 
contraction  of  the  ventricle.  As,  however,  extra-systoles  may  occur  with 
no  audible  sound,  this  distinction  is  not  reliable.  In  tracings  of  the  radial 
pulse  alone,  Wenckebach  ^^^  was  able  to  recognize  the  nature  of  the  irregu- 
larity by  an  ingenious  method  of  measurement.  No  difficulty  is  presented, 
as  a  general  rule,  when  tracings  of  the  radial  pulse  or  apex  beat  are  taken  at 
the  same  time  as  tracings  of  the  jugular  pulse.  The  slighter  forms  of  this 
affection  are  recognized  by  the  delay  that  occurs  between  the  auricular  and 
ventricular  systoles.  In  the  jugular  tracings,  as  has  already  been  shown, 
there  is  usually  present  a  wave  due  to  the  auricular  systole,  (a)  followed 
at  a  short  interval  by  the  carotid  wave  (c).  This  interval  between  a  and  c  is 
of  great  value  in  estimating  the  condition  of  the  conductivity  in  the  primitive 
tissue. 

§163.  The  intersystolic  period  (a-c  interval) — This]  interval]' is 
occupied  by  three  events,  namely,  (1)  the  systole  of  the  auricle  ;  (2)  the 
transmission  of  the  stimulus  from  auricle  to  ventricle  ;  (3)  a  minute  portion 
of  time  during  which  the  ventricular  pressure  is  rising  before  opening  the 
semilunar  valves  {Anspannungszeit,  or  presphygmic  interval).  As  3  is 
practically  constant,  it  may  for  the  purpose  of  this  inquiry  be  ignored,  and 
assuming  that  the  stimulus  for  contraction  starts  on  its  way  to  the  ventricle 
at  the  beginning  of  auricular  systole,  any  variation  in  the  length  of  the 
a-c  interval  is  due  to  the  variation  of  the  rate  of  stimulus  conduction. 

In  normal  hearts  I  have  found  that  the  a-c  interval  is  fairly  constant, 
lasting  usually  one-fifth  of  a  second  (as  in  Fig.  44).  It  is  a  little  shorter  in 
frequent  action  of  the  heart. 


CONDUCTING  FUNCTION  OF  PRIMITIVE  CARDIAC  TISSUE  177 

§  164.   Depression   of    conductivity   without    arrhythmia While 

the  a-c  interval  may  be  considered  normal  when  it  does  not  exceed  one-fifth 
of  a  second,  considerable  increase  of  this  interval  may  take  place  with  no 
interference  with  the  rhythm  of  the  heart. 


Fig.  111.     Shows  a  great  increase  in  the  a-c  interval  (space  A)  due  to  a  delay  in  the 
stimulus  passing  from  auricle  to  ventricle.    (Case  17,  Appendix  IV,  taken  1892.) 

In  Fig.  Ill  there  is  a  tracing  of  the  jugular  pulse  taken  at  the  same 
time  as  the  radial  pulse.  The  radial  shows  a  perfectly  regular  rhythm, 
while  the  neck  tracing  shows  a  great  increase  in  the  a~c  interval  (space  A). 
The  heart  may  continue  to  beat  perfectly  regularly  for  years  with  the 


Fig.  112.  Shows  an  increased  a-c  interval,  nearly  two-fifths  of  a  second  in  dura- 
tion (space  A).  The  shading  shows  the  position  of  the  murmurs — a  short  murmur 
due  to  the  auricular  systole,  the  loudest  part  of  which  is  separated  from  the  first 
sound  by  a  brief  interval,  a  murmur  following  the  first  sound,  and  another  following 
the  second  sound  running  up  to  the  presystohc  (or  auricular  systolic)  murmur. 
(Case  17,  Appendix  IV,  taken  1903.) 

conductivity  afEected  to  this  extent.  Thus,  Fig.  112  was  taken  in  1903 
from  the  same  patient  from  whom  Fig.  Ill  was  taken  in  1892,  and  the 
jugular  tracing  shows  a  hke  increase  of  the  a-c  interval  (space  A).  Except 
for  a  short  period  in  1898,  this  patient's  pulse  was  quite  regular  up  to  1904. 
§  165.    Influence  of  rest  upon  conductivity. — With  each  contraction 


MACKE.s'ZIU 


N 


178 


DISEASES  OF  THE  HEART 


all  the  functions  of  the  muscle-fibres  are  for  the  time  being  abolished,  to 
be  gradually  restored  during  diastole.  Normally,  their  recovery  is  simul- 
taneous, so  that  when  the  rhythmical  stimulus  arises  at  the  auricle  or  great 
veins  it  passes  over  the  whole  heart,  and  the  muscular  fibres  respond  at 
a  uniform  time.  When  one  of  these  functions  is  depressed,  its  recovery 
does  not  take  place  as  speedily  as  the  others,  therefore  the  relationship  of 
the  action  of  these  functions  is  not  uniform,  and  an  interference  with  the 
regular  sequence  of  events  results.  Certain  variations  in  the  rate  of  con- 
duction can  frequently  be  detected,  not  only  when  conductivity  is  depressed^ 
but  also  when  it  is  presumably  normal,  such  variations  apparently  depending 
on  the  time  required  for  recovery  after  the  previous  exhaustion.  One  has 
little  difficulty  in  illustrating  this  in  a  variety  of  ways  in  certain  forms  of 
heart  irregularity.     In  a  patient  aged  24,  suffering  from  mitral  disease, 


Fig.  113.  Shows  the  influence  of  rest  when  the  conductivity  of  the  a.-v.  fibres  is  depressed. 
The  radial  pulse  shows  a  respiratory  irregularity.  The  carotid  and  jugular  tracings  show 
a  shortening  of  the  a-c  interval  (space  A,^)  after  the  long  diastolic  periods,  and  a  lengthening 
(space  ^j)  after  the  short  diastolic  period  of  the  cardiac  cycle. 

and  pregnant  with  her  first  child,  I  had  noted  an  increase  in  the  a-c  interval 
for  some  years.  During  labour  it  frequently  happens  that  the  pulse  becomes 
irregular,  the  irregularity  often  being  of  a  respiratory  type  (sinus  irregularity). 
The  radial  tracing  in  Fig.  113  shows  such  an  irregularity.  The  tracing  of 
the  carotid  and  jugular  shows  a  rise  and  a  fall  due  to  the  movements  of 
respiration — the  rise  in  the  tracing  corresponding  with  expiration,  and  the 
fall  with  inspiration.  It  will  be  noted  that  the  irregularity  is  due  to  a 
lengthening  of  the  diastole,  and  that  the  a-c  interval  during  the  short  pulse 
period  (space  A^)  is  nearly  double  the  duration  of  the  a-c  interval  during  the 
long  pulse  period  (space  A.^)-  The  reason  for  this  variation  in  the  a-c  interval 
is  that  the  conductivity  is  continually  depressed,  but  when  the  heart  beats  at 
a  slower  rate  the  a.-v.  fibres  have  time  to  recover  during  the  longer  diastolic 
pause,  so  that  the  stimulus  is  conveyed  from  auricle  to  ventricle  at  about 
the  normal  rate  [A^).  Here  the  arrhythmia  is  not  due  to  the  depressed 
conductivity,  but  evidently  originates  in  the  sinus,  for  the  auricular  wave, 


CONDUCTING  FUNCTION  OF  PRIMITIVE  CARDIAC  TISSUE     179 

a,  appears  at  irregular  intervals.  The  modifying  effect  on  the  ventricular 
rhythm  of  the  variable  condition  of  the  conductivity  can  be  illustrated  in 
a  variety  of  ways.  If  we  examine  minutely  the  incidents  where  an  occasional 
premature  or  extra  systole  occurs,  sometimes  very  curious  variations  in 
conductivity  can  be  detected  (as  in  Fig.  106,  Plate  II;  also  Figs.  274,  and 
265  Plate  V). 

It  may  seem  an  unnecessary  refinement  to  dwell  upon  such  minute 
changes,  but  I  trust  to  show  later  that  the  recognition  of  these  facts  affords 
the  evidence  for  determining  with  certainty  some  changes  of  the  utmost 
significance  in  a  large  class  of  cases  of  heart  disease. 

§  1 66.    Arrhythmia    due    to    depression    of    conductivity Slight 

arrhythmia  may  be  due  to  variations  of  conductivity.     Thus  the  short  space 


Fig.  114.  Shows  a  gradual  lengthening  of  the  a-c  interval  tiU  the 
stimulus  from  the  auricle  at  a'  reaches  the  a. -v.  bundle  before  the  latter 
has  recovered  from  the  previous  stimulation,  and  finds  it  '  refractory '. 
The  ventricle,  therefore,  does  not  respond  to  this  stimulus,  but  remains 
quiescent  till  the  next  physiological  stimulus  comes  from  the  auricle,  and 
the  conductivity  being  restored  the  ventricular  beat  (c)  follows  the 
auricular  wave  at  a  shorter  interval.  Note  the  increasing  size  of  the 
a  wave  before  the  intermission.  This  is  due  to  the  auricular  systole 
falling  at  the  same  time  as  the  preceding  ventricular  systole,  so  that  the 
auricular  contents  cannot  be  sent  into  the  ventricle,  but  a  bigger  wave  is 
sent  back  into  the  veins. 

o  in  the  radial  in  Fig.  98  is  seen  to  be  due  to  an  increase  of  the  preceding 
a-c  interval  (space  A^),  that  is,  to  a  delay  in  the  ventricular  systole. 

Arrhythmia  of  a  more  marked  character  arises  when  the  conductivity 
is  so  grievously  depressed  that  the  stimulus  occasionally  or  frequently  fails 
to  cross  the  auriculo-ventricular  junction.  How  this  occurs  is  well  seen 
in  Fig.  114.  There  is  a  constant  delay  in  the  conduction  of  the  stimulus 
here,  the  a-c  interval  being  unduly  prolonged.  Before  the  intermission 
there  is  a  slight  but  gradual  increase  of  the  a-c  interval.  After  the  auricular 
wave  a'  there  is  no  carotid  wave  (c)  nor  pulse  beat  in  the  radial.  The  reason 
for  this  is  manifestly  that  the  auricular  systole  a'  occurred  so  soon  after  the 
previous  ventricular  systole  (as  evidenced  by  the  carotid  wave  c  immediately 
before  a')  that  there  was  not  sufficient  time  for  the  recovery  of  the  function 

N  2 


180 


DISEASES  OF  THE  HEART 


of  stimulus  conduction  in  the  a. -v.  bundle,  and  hence  the  stimulus  failed  to 
reach  the  ventricle,  and  a  beat  dropped  out.  By  this  means  a  longer  rest 
was  procured  for  these  fibres,  and  when  the  next  stimulus  comes  down  from 


Fig.    115.     Regularly  intermitting  pulse  due  to  depression  of  conductivity. 
(Case  17,  Appendix  IV,  1898.) 

the  auricle  the  longer  rest  has  so  restored  the  function  of  conductivity 
that  the  a-c  interval  following  the  pause  is  shorter  than  the  average.  This 
dropping  out  of  ventricular  beats  may  occur  at  regular  intervals.  Fig.  115 
was  taken  in  1898  from  the  patient  from  whom  Figs.  1 1 1  and  112  were  taken. 


Fig.  116.  Taken  at  the  same  visit  as  Fig.  115,  and  shows  the  venous  pulse  during  the 
arrhythmia.  The  wave  a  is  quite  regular  in  its  appearance.  For  the  interpretation  of  this 
tracing  see  diagram  Fig.  117. 

For  many  years  tracings  from  this  patient  showed  constant  depression  of 
the  conductivity.  For  some  reason,  in  1898  the  conductivity  became 
further  depressed,  so  that  at  regular  intervals  a  ventricular  beat  dropped  out 
(Fig.  115).     The  true  nature  of  this  arrhythmia  is  shown  in  the  jugular  tracing 


Fig.  117.  Diagram  constructed  to  show  that  the  irregularity  in  Figs.  115 
and  116  is  due  to  a  blocking  of  the  conductivity  at  the  fibres  joining  auricle  and 
ventricle.  Note  the  increased  length  of  the  a-c  interval  before  the  pause  in 
the  Vs. 

(Fig.  116),  where  the  auricle  is  shown  to  contract  regularly  (wave  a),  while 
the  ventricle  fails  to  respond  to  every  third  auricular  systole.  To  demon- 
strate this  more  clearly,  I  reconstruct  Fig.  116  in  the  form  of  a  diagram 
(Fig.  117).     The  downstrokes  in  the  upper  division  represent  the  auricular 


CONDUCTING  FUNCTION  OF  PRIMITIVE  CARDIAC  TISSUE   181 


systole  {As),  those  in  the  lowest  the  ventricular  systoles  {Vs),  and  correspond 
with  the  radial  and  carotid  pulses  in  Figs.  115  and  116.  The  slanting  lines 
represent  the  a-c  interval.  It  will  be  seen  that  a  ventricular  beat  drops 
out  regularly  after  every  third  auricular  systole. 

§  167.  Missed  beats  due  to  depression  of  conductivity. — Gaskelli-^ 
states   that   on  applying  a  screw  clamp   around   the   auriculo-ventricular 


Fig. 


118.     The  ventricle  only  responds  to  every  alternate  auricular  systole 
ventricular  rate  48,  auricular  rate  96. 


groove  of  a  frog's  heart,  '  according  to  the  tightness  of  the  clamp  the  ventricle 
can  be  made  to  beat  synchronously  with  the  auricles,  to  respond  to  every 
second  contraction  of  the  auricle,  to  respond  to  every  third,  fourth,  or 
other  contraction,  or  to  remain  quiescent.'  Hering^^^  and  Erlanger^'^  have 
recently  produced  the  same  changes  in  the  mammalian  heart.  All  these 
varying  results  can  be  demonstrated  to  occur  in  the  human  heart. 


ac       a 

UM\ ^^ 


-^    RaHidl 


Fig.  119.  Is  from  a  slow,  irregular  pulse  after  influenza,  and  the  jugular  tracing  shows 
that  the  slow  pulse  is  due  to  the  ventricle  failing  to  respond  to  the  stimulus  from  the  auricle. 
Note  that  after  the  short  pulse  period  in  the  radial  the  a-c  interval  is  much  longer  than  at  the 
other  periods.  This  is  because  the  fibres  have  had  a  short  rest,  and  the  conductivity  has  in 
consequence  not  been  completely  restored.  Note  also  at  a;  a  slight  depression  in  the  radial 
tracing  due  to  the  systole  of  the  left  auricle  affecting  the  arterial  column  (see  Fig.  120). 

In  Fig.  114  the  ventricular  systole  is  seen  to  drop  out  at  rare  intervals  ; 
in  Fig.  116  the  ventricular  systole  drops  out  after  every  third  auricular 
systole  (3:2  rhythm)  ;  in  Fig.  118,  after  every  second  (2:1  rhythm).  In 
Fig.  119  the  ventricular  systole  usually  drops  out  after  every  second  auricular 
systole  ;  but  there  is  one  short  pulse  period,  and  the  a-c  interval  here  is  much 
longer  than  the  a-c  period  after  the  longer  periods,  the  lengthening  being 
an  evidence  that  the  conducting  power  of  the  auriculo-ventricular  fibres 
has  not  had  time  to  recover  as  effectually  as  after  the  longer  pulse  periods 


182 


DISEASES  OF  THE  HEART 


(see  diagram,  Fig.  120).  In  Fig,  121  there  are  three  auricular  contractions 
to  one  ventricular  (3:1  rhythm),  except  during  the  last  arterial  pulse-period, 
when  there  are  but  two  auricular  waves,  and  after  the  second  of  these  the 
a-c  interval  is  longer  than  the  other  a-c  intervals  in  this  tracing. 

In  tracings  published  by  G.  Gibson  ^,  Hay  ^^^,  and  Beards  ^^^,  there  are 
four  auricular  beats  to  one  ventricular.  This  blocking  may  be  so  extreme 
that  the  auricle  may  beat  ten  or  twelve  times  and  the  ventricle  stand  stiU. 


Fia.  120.  Diagram  of  Fig.  119,  showing  the  blocking  of  the  stimulus  after  every  second  auricular 
systole,  except  in  one  instance  when  it  gets  through,  with  a  lengthened  a-c  interval. 

§  1 68.  Independent  ventricular  rhythm  due  to  heart-block. — In 

the  tracings  I  have  given  so  far,  it  could  be  shown  that  when  the  ventricle 
does  contract  it  is  in  response  to  a  stimulus  from  the  auricle.  When  a  ligature 
is  applied  in  the  auriculo-ventricular  groove  of  the  frog's  heart,  so  that  the 
stimulus  can  be  conveyed  no  longer  from  auricle  to  ventricle,  the  latter  beats, 
after  a  time,  with  a  rhythm  different  from,  and  independent  of,  that  of  the 
auricle     (complete    heart-block).     Wooldridge    and    Tigerstedt    produced 


Fig.  121.  Here  the  tracing  from  the  neck  shows  sometimes  three  auricular  waves  (o)  to 
one  carotid  wave  (c).  In  the  last  two  periods  there  are  but  two  auricular  waves,  and  the 
a-c  interval  is  longer  than  in  the  periods  when  there  are  three  auricular  waves,  because  in  the 
former  case  the  conductivity  has  not  had  so  long  a  time  to  be  restored. 

complete  independence  of  the  auricular  and  ventricular  rhythms  by 
physiologically  separating  the  auricles  from  the  ventricles,  while  a  similar 
result  has  been  attained  by  His,  jr.,  Hering  and  Erlanger  through  compres- 
sion of  the  a.-v.  bundle.  Erlanger  2-2  has  produced  complete  heart-block 
experimentally  in  dogs,  and  the  dogs  have  lived  for  many  months,  with 
symptoms  identical  with  those  found  in  human  subjects  suffering  from 
heart-block.  This  independent  rhythm  can  be  demonstrated  as  the  cause 
of  certain  forms  of  a  slow  pulse-rate  in  the  human  subject.  Fig.  122  is 
a  tracing  of  the  radial  taken  at  the  same  time  as  the  pulsation  in  the  neck 


CONDUCTING  FUNCTION  OF  PRIMITIVE  CARDIAC  TISSUE     183 

due  to  the  jugular  and  carotid.  The  small  waves,  a,  are  due  to  the  right 
auricle,  and  there  are  two  of  these  auricular  waves  to  one  carotid  or  radial 
pulse  beat.  But  when  one  carefuUy  analyses  their  relationship,  it  is  found 
that  the  two  auricular  periods  are  less  than  one  ventricular  period,  so  that  the 


Fig.  122.    Shows  complete  heart-block,  the  auricle  pursuing  one  rhythm,  and  the  ventricle 

another  and  slower  rhythm. 

relationship  of  the  auricular  systole  to  the  ventricular  systole  is  a  constantly 
varying  one,  sometimes  at  a  distance,  and  then  gradually  approaching  till 
they  are  synchronous.  Whatever  relationship  the  a  has  to  c,  no  variation 
takes  place  in  the  rate.     The  same  thing  is  shown  in  Fig.  123,  where  the  apex 


Fig.  123.  From  the  same  case  as  Fig.  122.  Shows  the  influence  of  the  left  auricle  on  the 
apex  tracing  (wave  a).  In  the  radial  tracing  the  dips  (  x )  due  to  left  auricle  are  found  to  occur 
immediately  after  the  auricular  waves  in  the  apex  tracing. 

beat  is  recorded  at  the  same  time  as  the  radial.  Here  there  is  a  small  wave, 
a,  due  to  the  systole  of  the  left  auricle,  and  the  same  maintenance  of  indepen- 
dent rhythms  is  manifest  here.  One  can  infer  with  certainty  that  the  auricle 
contracted  at  the  same  time  as  the  ventricular  systole  during  the  first  four 


184  DISEASES  OF  THE  HEART 

or  five  of  the  ventricular  apex  beats,  but  that  the  evidence  of  this  simul- 
taneous contraction  is  obscured  by  the  large  ventricular  wave,  for  we  can 
see  in  Fig.  122  how  the  wave  a  occurred  at  the  same  time  as  the  carotid 
wave.  I  have  taken  a  large  number  of  tracings  from  this  patient  at  various  • 
times  and  under  various  circumstances,  and  I  have  invariably  found  the 
independence  of  rhythm  between  the  auricle  and  ventricle. 

§  169.  Effect  of  the  auricular  contraction  on  the  radial  pulse. 
— The  auricular  systoles  can  sometimes  be  recognized  in  another  way  in 
tracings  of  the  radial  pulse,  where,  during  a  long  ventricular  pause,  a  series 
of  notches  can  be  seen  occurring  at  regular  intervals  on  the  descending 
line  of  the  radial  tracing,  as  in  Fig.  124.  If  a  jugular  tracing  be  taken  at 
the  same  time,  there  wiU  be  found  auricular  beats  occurring  exactly  at  the 
same  time  as  these  notches,  as  is  shown  in  Figs.  119,  122,  and  123.  From 
this  I  suggest  that  those  notches  in  Fig.  124  are  due  to  the  movement  of  the 


Fig.  124.     From  Webster's  case  of  heart-block,  showing  in  the  falling  line  of    the    radial 
tracing  a  series  of  interruptions  (a)  due  to  the  left  auricle. 

left  auricle,  the  systole  of  the  left  auricle  pressing  against  the  aortic  valves 
temporarily  affecting  the  arterial  column.  The  sudden  cessation  of  this 
pressure  causes  a  slight  but  abrupt  fall  in  the  aortic  pressure,  giving  rise 
to   the   notches   in  the  radial  tracing. 

§  170.  Etiology. — Except  in  cases  of  complete  heart-block,  the  ana- 
tomical changes  have  not  been  fully  worked  out.  In  the  majority  of  the 
cases  of  heart-block  examined  post  mortem,  damage  of  the  a.-v.  bundle  at 
or  beyond  the  a.-v.  node  has  been  found,  due  to  acute  inflammatory  changes 
or  to  sclerotic  changes,  or  to  the  presence  of  gummata.  In  the  milder  cases 
one  can  only  infer  the  cause.  From  Gaskell's  experiments  we  know  that 
if  the  bridge  of  muscle  connecting  the  auricle  and  ventricle  be  narrowed, 
the  stimulus  takes  longer  in  passing.  We  know  also  that  in  rheumatic 
affections  of  the  heart  numerous  deposits  of  cells  occur  in  the  muscle  sub- 
stance. As  it  is  in  rheumatic  heart  cases  and  cardio-sclerosis  that  I  have 
found  most  of  the  milder  forms  of  depressed  conductivity,  I  infer  that 
when  such  deposits  occur,  or  when  a  slight  cicatrization  takes  place,  the 
bundle  is  injured,  and  so  the  function  of  conductivity  is  impaired.  In 
other  acute  affections  of  the  heart  we  get  evidence  of  the  implication  of  this 


CONDUCTING  FUNCTION  OF  PRIMITIVE  CARDIAC  TISSUE     185 

bundle  in  the  diseased  process  (see  Chapter  XXIV).  Little  is  known  as  regards 
complete  heart-block  as  an  acute  condition,  but  I  refer  to  its  possibility  in 
febrile  affections  of  the  heart,  and  one  case  has  been  recorded  by  Jelhnek 
and  Cooper  ^°i  with  confirmatory  post-mortem  details.  In  cardio-sclerosis  we 
may  observe  symptoms  of  impaired  conductivity  and  even  heart-block  in 
an  individual  who  has  shown  extra-systoles  and  the  nodal  rhythm. 

The  sclerotic  changes  in  the  heart  muscle  associated  with  arterio-sclerosis 
of  the  coronary  arteries  appear  likely  to  be  the  most  common  cause  of 
heart-block.  If  one  looks  at  Fig.  2,  it  will  be  seen  how  the  a. -v.  bundle  passes 
through  the  central  fibrous  body  of  the  heart.  This  body  is  composed,  of 
fibrous  tissue,  and  is  the  fixed  point  in  which  are  inserted  many  of  the  muscular 
fibres  of  the  ventricle,  and  from  this  place  sclerotic  changes  are  apt  to 
spread.  Further,  Keith's  researches  into  the  hearts  I  have  sent  him  have 
shown  that  the  sclerotic  process  is  apt  to  extend  from  the  base  of  the  mitral 
valve  into  the  central  fibrous  body,  and  to  involve  the  bundle.  I  have 
suggested  this  as  a  probable  cause  for  the  production  of  extra-systoles  and 
the  nodal  rhythm,  and,  in  certain  advanced  cases,  of  heart-block. 

Several  cases  have  been  reported  where  the  damage  to  the  bundle  was 
due  to  gummata,  and  the  recovery  of  other  cases  under  anti-syphilitic 
treatment  indicate  that  syphilis  may  be  an  agent  in  the  production  of  com- 
plete heart-block.  Bramwell^^^  has  recently  reported  a  case  of  complete 
heart-block  in  a  rheumatic  heart,  and  I  have  found  that  sHght  impairment 
of  the  bundle  in  rheumatic  hearts,  especially  with  mitral  stenosis,  is  not 
infrequent. 

In  complete  heart-block  the  a. -v.  node  may  be  either  destroyed  or  sepa- 
rated from  the  remainder  of  the  a. -v.  bundle.  The  remains  of  the  bundle 
in  the  ventricle  beyond  the  a. -v.  node  have  been  found  perfectly  normal 
in  a  case  described  by  Keith  in  which  there  was  a  history  of  complete  heart- 
block  for  eighteen  years.  Seeing  that  the  bundle  was  healthy,  it  must  have 
had  some  function  during  life,  and  as  it  did  not  convey  stimuH  from  auricle 
to  ventricle,  it  must  have  had  some  other  function,  which  I  suggest  was 
stimulus  production,  and  the  maintenance  of  the  slow  ventricular  rate. 

There  is  a  great  defect  in  our  knowledge  of  the  condition  leading  up  to 
heart-block.  Before  the  slow  ventricular  rhythm  becomes  permanent,  in 
many  people  there  are  periods  in  which,  though  the  rhythm  of  the  heart 
is  normal,  there  is  frequently  an  increased  a-c  interval ;  and  at  times  ventri- 
cular systoles  drop  out  at  intervals  more  or  less  regular  and  frequent.  I  am 
convinced  that  in  some  cases  there  is  a  connexion  between  the  conditions 
producing  the  nodal  rhythm  and  heart-block,  I  have  reasoned  that  most 
cases  of  nodal  rhythm  are  due  to  degeneration  or  irritation  of  the  a. -v.  node, 


186  DISEASES  OF  THE  HEART 

while  a  few  may  be  due  to  a  break  between  the  sinus  remains  and  the  a. -v. 
node  on  account  of  the  atrophy  of  the  auricular  wall  from  long-continued 
distension.  The  mischief  causing  the  nodal  rhythm  and  the  independent 
ventricular  rhythm  of  heart-block  is  thus  seen  to  be  very  near.  I  cite  fully 
in  the  Appendix  (IV)  cases  of  nodal  bradycardia  having  some  affinity  to 
heart-block.  In  one  there  was  for  years  an  increased  a-c  interval,  and  at 
one  period  a  mild  heart-block,  and  finally  a  nodal  rhythm  of  a  very  slow 
character  (Case  17,  Appendix  IV). 

The  possibility  of  vagal  stimulation  taking  part  in  the  production  of 
heart-block  must  be  borne  in  mind.  Stimiilation  of  the  vagus  can  produce 
a  similar  action  of  the  heart,  as  Chauveau  2^' pointed  out.  Roy  and 
Adami  ^^^  give  excellent  tracings  showing  complete  heart-block  due  to  direct 
stimulation  of  the  vagus  and  to  the  administration  of  muscarin.  I  give 
tracings  where  a  mild  form  of  heart-block  was  produced  by  a  reflex  stimula- 
tion of  the  vagus  by  swallowing  (Case  27,  Appendix  VI).  Digitahs  may 
also  produce  it.  But  in  these  cases  there  is  evidence  of  a  defect  of  the  a. -v. 
bundle — in  the  permanent  delay  of  conduction.  In  Webster's  ^^e  Q^^gg  i\^q 
arrest  of  the  ventricle  arose  in  two  ways,  as  Wenckebach's  ^^^  masterly 
analysis  brings  out,  and  one  of  these  ways  points  to  vagus  stimulation. 

§  171.  Significance  of  the  milder  forms  of  depression  of  con- 
ductivity— It  must  not  be  thought  that  the  foregoing  data  are  merely 
of  academic  interest.  Their  recognition  and  appreciation  clear  up  many 
obscurities  surrounding  heart  affections,  and  are  of  practical  importance  in 
treatment.  As  will  be  shown,  in  acute  affections  of  the  heart  the  presence  of 
the  irregularity  due  to  this  cause  indicates  that  the  muscle  is  being  invaded 
by  the  disease.  When  it  occurs  without  any  irregularity,  the  increased 
a-c  interval  is  of  importance  in  the  administration  of  such  drugs  as  digitaUs. 
I  have  rarely  failed  in  such  cases  in  increasing  the  a-c  interval  and  causing 
the  dropping  out  of  ventricular  systoles  by  the  administration  of  digitalis, 
and  the  recognition  of  this  form  of  irregularity  produced  by  digitafis  is  of 
importance,  for  digitahs  should  never  be  pushed  further.  One  reads  of 
accounts  of  sudden  death  during  or  after  the  digitalis  had  slowed  the  pulse, 
and  it  has  seemed  to  me  that  the  immediate  cause  might  be  the  production 
of  severe  heart-block  and  consequent  syncope.  I  have  a  few  times  seen 
in  consultation  patients  whose  hearts  were  greatly  slowed  by  excessive 
doses  of^digitahs,  but  at  that  time  I  had  not  acquired  the  means  of  recog- 
nizing the  cause.  I  always  make  it  a  rule  to  stop  digitalis  as  soon  as  I  find 
the  pulse  dropping  a  beat  (see  §  252).  The  recognition  of  the  cause  of  the 
intermission,  as  in  Fig.  115,  should  always  be  an  indication  against  the  use 
of  digitalis. 


CONDUCTING  FUNCTION  OF  PRIMITIVE  CARDIAC  TISSUE     187 

§  172.  Symptoms   associated    with    heart-block Apart  from   the 

characteristic  irregularity,  and  the  slow  ventricular  rhythm  with  its  asso- 
ciated syncopal  attacks,  there  are  no  characteristics.  Patients  with  a 
pulse-rate  of  thirty  to  forty  beats  per  minute  may  go  about  their  affairs, 
but  quietly — the  field  of  response  being  distinctly  hmited.  The  manner  of 
limitation  is  varied  :  in  some  it  is  a  sense  of  weakness,  in  others  exertion 
induces  attacks  of  dyspnoea — sometimes  extremely  violent  on  very  slight 
exertion.  The  picture  given  by  the  late  Sir  W.  T.  Gairdner,  a  sufferer 
from  heart-block,  of  his  own  experiences,  is  very  characteristic  of 
some  cases.  '  I  am  wonderfully  free  ' — he  wrote  me  four  years  after 
the  slow  rhythm  began,  and  two  years  before  his  death  at  the  age  of 
eighty-two,  his  pulse-rate  then  being  thirty  per  minute — '  from  all  the 
symptoms  that  usually  go  along  with  organic  heart-disease.  My  sleep  is 
almost  always  undisturbed,  and  I  get  abundance  of  it  both  by  day  and  night, 
nor  is  there  the  slightest  trace  of  angina  pectoris,  severe  dyspnoea,  dropsy, 
or  any  of  the  usual  accidents  of  prolonged  cardiac  disease.'  He  wrote  later  : 
*  Although  a  little  uncertain  in  my  gait,  I  can  go  from  one  room  to  another 
or  even  up  a  simple  stair,  taking  plenty  of  time  and  assisted  by  the  railing  ; 
but  for  the  last  two  years  at  least,  if  not  more,  my  position  has  been  with 
few  exceptions  recumbent,  or  at  most  sitting,  and  repeated  attempts  have 
shown  me  that  it  is  practically  impossible  to  cross  the  street  or  to  go  into  the 
garden  opposite  the  house  except  in  a  wheeled  armchair  ;  and  along  with  this 
there  is  a  feeling  of  perpetual  weariness  which  never  leaves  me  even  after 
the  soundest  sleep,  and  which  is  not  explained  by  any  pain  or  suffering, 
though  in  itself  it  often  tends  to  fits  of  yawning  and  even  exclamations 
which  would  sound  to  others  as  if  I  was  suffering  inwardly  '  (see  also  Gibson 
and  Ritchie's  232  description  of  this  case). 

The  syncopal  and  epileptiform  attacks  due  to  cerebral  anaemia  induced 
by  the  slow  action  or  temporary  stoppage  of  the  ventricles  (Adams-Stokes 
syndrome)  have  been  described  on  p.  24.  This  tendency  to  infrequent 
action  may  appear  in  affections  of  the  bundle  at  two  stages,  namely,  before 
the  permanent  establishment  of  the  independent  ventricular  rhythm  and 
after  its  establishment.  While  there  are  intermittent  periods  of  temporary 
heart-block,  there  is  a  certain  hability  to  these  syncopal  attacks,  and  the 
following  appears  to  me  to  be  the  reason.  After  a  Stannius'  ligature  is 
applied  between  auricle  and  ventricle,  the  ventricle  stands  still  for  a  longer  or 
shorter  period  before  it  starts  on  its  own  rhythm.  In  certain  cases  of  heart- 
block  the  stimulus  to  contraction  passing  from  auricle  to  ventricle  may  sud- 
denly stop,  and  the  ventricle  pause  for  a  brief  period  before  it  starts  its  own 
contraction.   It  is  during  this  period  that  the  syncopal  attacks  occur.    Thus, 


188  DISEASES  OF  THE  HEART 

Sir  W.  T.  Gairdner  noticed  that  his  attacks  always  came  on  with  the  sudden 
dropping  of  his  pulse-rate  :  '  These  cardiac  and  cerebral  attacks  were  at  one 
time  so  frequent  that  I  think  from  twenty  to  thirty  of  them  were  numbered 
in  twenty-four  hours.'  His  pulse-rate  would  be  seventy  per  minute,  and  after 
his  syncopal  attack  he  invariably  found  it  at  or  below  thirty  per  minute. 
When  the  pulse  subsided  to  a  permanent  rate  of  twenty  to  thirty  per  minute, 
the  cerebral  attacks  disappeared.  My  reading  of  this  description  is  that 
while  the  block  was  partial  the  stimulus  at  times  got  through  from  the 
auricle  and  the  rate  of  the  pulse  rose  to  seventy  ;  then  the  stimulus  suddenly 
failed  to  get  through,  and  the  ventricle  paused  for  a  brief  period  as  it  does 
on  first  applying  the  Stannius'  ligature,  anaemia  of  the  brain  resulted,  and 
the  patient  fainted.  On  the  ventricle  starting  its  own  rhythm  the  circula- 
tion of  the  brain  was  restored,  and  the  patient,  recovering,  found  his  pulse 
at  the  rate  of  thirty  per  minute.  When,  however,  the  block  became  perma- 
nent, the  ventricle  went  on  at  its  slow,  independent  rate,  with  no  pauses 
and  therefore  with  no  syncopal  attacks.  From  tracings  taken  during 
attacks  of  syncope,  Wenckebach  and  Gossage  have  shown  that  the  cerebral 
anaemia  may  arise  by  the  ventricle  suddenly  beating  with  great  rapidity, 
the  individual  contractions,  however,  being  so  small  that  the  brain  is  not 
sufficiently  supplied  with  blood. 

Syncopal  attacks  may  appear  when  the  rate  is  constant  at  thirty  and 
under.  In  such  cases  there  is  invariably  a  greater  slowing  of  the  heart's 
action,  the  rate  falUng  sometimes  as  low  as  five  beats  per  minute.  This 
point  is  well  brought  out  in  the  tracings  from  patients  during  an  attack 
taken  by  Webster  3-^,  Hay  ^^^,  and  Barr  ^^^^  The  immediate  cause  of  the 
greater  slowing  is  not  understood. 

I  have  only  seen  a  patient  recovering  from  an  attack,  and  I  take  the 
following  description,  which  seems  fairly  representative,  from  Hay  and 
Moore's  '^^^  description  : — 

'  He  was  sitting  up  in  bed  when  suddenly  another  attack  seized  him  ;  no 
sooner  had  he  recovered  and  spoken  a  few  words,  than  he  was  again  attacked. 
He  made  one  or  two  hurried  respirations,  his  head  fell  on  his  breast,  and  he 
sank  on  to  his  piUow,  breathing  stertorously  ;  his  cheeks  and  alae  nasi  flapped 
in  and  out  ;  he  ceased  breathing,  his  eyes  closed,  but  his  pupils  were  widely 
dilated,  and  his  eyeballs  were  turned  upwards  and  to  the  left.  His  face  was 
ashen  grey,  the  malar  flush  had  vanished,  and  he  had  all  the  appearance 
of  a  corpse.  In  a  little,  however,  the  colour  gradually  returned  to  his  face, 
he  sighed  deeply  and  woke  up.  He  raised  himself  a  little,  stared  about, 
and  then  sank  back  on  the  pillows  exhausted  and  sweating.  During  the 
seizure  the  radial  pulse  could  not  be  felt  until  just  before  the  return  of 
consciousness.' 

In  other  descriptions  epileptiform  movements  are  also  included. 


CONDUCTING  FUNCTION  OF  PRIMITIVE  CARDIAC  TISSUE     189 

From  the  patient's  sensations  of  an  attack,  I  quote  the  following 
letter  written  by  an  old  friend  of  mine  who  suffered  from  Adams-Stokes 
syndrome  due  to  nodal  bradycardia,  the  pulse-rate  usually  being  thirty  per 
minute: —  ' 

'  At  your  request  I  try  to  give  you  a  description  of  an  extraordinary 
swoon  I  had  whilst  suffering  under  heart  trouble.  It  happened  in  the  middle 
of  the  night.  I  awoke  from  a  quiet  sleep  feeling  a  most  curious  creepy 
sensation  ;  my  functions  all  seemed  to  be  stopping,  and  in  front  of  me,  about 
two  feet  from  the  floor,  appeared  a  circular  light  about  two  inches  in  diameter, 
and  brilliant  beyond  anything  I  had  ever  seen  before.  I  thought  the  period 
of  my  dissolution  had  arrived.  I  was  perfectly  calm,  and  I  began  to  reason 
with  myself  whether  I  should  waken  my  wife  (I  don't  know  whether  I  should 
have  had  strength  ;  I  was  turned  from  her  at  the  time),  in  which  case  she 
would  be  greatly  alarmed,  or  leave  things  to  take  their  course.  Before  my 
mind]was  made  up  what  to  do,  the  light  began  to  contract,  and  when  it  was 
reduced  to  about  half  its  original  size  suddenly  went  out,  but  before  entirely 
losing  consciousness  I  had  such  a  feeling  of  peace  and  restfulness  as  I  never 
experienced  before,  and  had  just  time  to  say  to  myself,  "  There  is  no  after- 
life anyway." 

'  How  long  I  lay  in  that  condition  of  course  I  don't  know,  but  when  I  did 
come  to,  I  felt  it  utterly  impossible  to  move  :  I  might  have  been  a  leaden 
image,  I  felt  such  a  weight.  For  a  long  time  I  persevered  in  trying  to  move 
a  limb.  At  last  I  got  a  little  life  in  one  of  my  feet,  and  then  gradually  the 
use  of  all  my  limbs.' 

Cheyne-Stokes  respiration  may  appear  in  patients  suffering  from  heart- 
block,  and  Gibson  and  Ritchie  ^^^  record  falls  of  arterial  pressure  during  the 
apnoeic  stage. 

A  curious  feature  in  cases  of  heart-block  is  that  circumstances 
that  usually  excite  the  heart  to  rapid  action  have  Uttle  effect  upon  the 
independent  ventricular  rhythm.  Causes  of  excitement,  and  the  ad- 
ministration of  alcohol  or  chloroform,  have  very  slight  or  no  effect  on  the 
ventricle,  though  the  auricular  contractions  may  be  rendered  much  more 
frequent. 

§  173.  Prognosis In  the  milder  cases  where  there  is  a  delay  in  the 

stimulus  passing  from  auricle  to  ventricle,  or  where  there  may  be  occa- 
sionally the  characteristic  irregularity  caused  by  the  dropping  out  of  a 
ventricular  systole,  no  grave  conditions  arise.  Its  recognition,  however,  warns 
us  that  myocardial  changes  are  involved,  and  the  susceptibility  of  the  patient 
to  the  digitalis  group  of  remedies  should  be  borne  in  mind.  Patients  with 
mild  forms  of  heart-block,  even  where  the  pulse  is  continuously  about  thirty, 
may  lead  quiet,  uneventful  lives  for  ten  or  twenty  years.  When  there  is 
a  tendency  to  syncopal  attacks,  then  the  patient's  life  is  uncertain,  as  such 
patients  usually  die  in  one  of  these  attacks,  often  being  found  dead  in  bed 


190  DISEASES  OF  THE  HEART 

or  elsewhere.  Death  may  arise  from  heart  failure,  preceded  by  symptoms 
of  oedema  of  the  lungs  and  dropsy. 

§  174'  Treatment. — We  occasionally  meet  with  cases  where,  after 
repeated  attacks  of  syncope  and  long-continued  slow  pulse,  the  conducting 
power  is  restored  and  the  rate  becomes  normal.  But  considering  the 
pathological  change  producing  these  cases,  it  will  be  reaUzed  how  futile  it 
is,  except  in  syphilitic  cases,  to  attempt  to  give  remedies  to  cure.  Notwith- 
standing this,  many  writers  prescribe  drugs  of  the  most  diverse  character — 
even  digitalis,  which  is  so  demonstrably  contra-indicated.  Fortunately 
for  the  patients  most  of  the  drugs  are  innocuous  so  far  as  the  heart  is  con- 
cerned. The  management  of  these  cases  should  be  directed  to  seeing  that 
the  patient  leads  a  life  according  to  his  strength,  avoiding  anything  that 
induces  over-exertion,  limiting  the  amount  of  food  to  what  is  necessary  for 
his  limited  way  of  living.  While  the  tendency  to  syncopal  attacks  is  present, 
extreme  care  should  be  taken  that  he  should  not  expose  himseK  to  the  attack 
occurring  in  dangerous  situations.  He  can  move  quietly  about  with  such 
attendance  as  his  means  can  afford. 

In  a  few  syphilitic  cases,  recoveries  have  been  effected  by  the  energetic 
use  of  anti-syphilitic  remedies. 


CHAPTER   XXII 

Exhaustion  of  Contractility 

§  175.  Necessity  for  recognizing  exhaustion  of  contractility 

176.  The  function  of  contractility. 

177.  Conditions  inducing  exhaustion  of  contractility. 

178.  Symptoms  :    (o)  reflex,  (b)  changes  in  the  heart's  action. 

179.  The  pulsus  alternans. 

180.  Prognosis. 

181.  Treatment. 

§  175.  Necessity  for  recognizing  exhaustion   of   contractility. — 

Seeing  that  the  cause  of  all  forms  of  heart  failure  finally  resolves  itself 
into  the  inabiUty  of  the  contractile  force  to  maintain  efficiently  the  circulation, 
it  is  necessary  to  describe  in  some  detail  the  part  played  by  the  failure  of 
contraction  alone.  While  it  is  true  that  heart  failure  may  be  induced  by  the 
disturbance  of  other  functions,  and  that  the  symptoms  produced  by  these 
commonly  dominate  the  situation— excessive  rapidity,  irregularity,  dilatation 
— there  are  also  signs  evoked  by  the  failure  of  contractility  which  are  often 
obscured  and  overlooked  in  the  confusion  created  by  more  pronounced  symp- 
toms, but  which  nevertheless  can  be  recognized  and  apportioned  to  their 
appropriate  cause.  We  sometimes  see  dyspnoea,  enlargement  of  the  liver, 
and  dropsy  described  as  the  cardinal  symptoms  of  heart  disease,  but  equally 
serious  conditions  of  heart  disease  and  heart  failure  may  be  present  with 
none  of  these  symptoms.  With  the  exception  of  dyspnoea,  the  '  cardinal ' 
symptoms  are  usually  associated  with  dilatation  of  the  heart,  i.  e.  failure 
of  tonicity.  Failure  of  contractility  may  occur  with  little  or  no  increase 
in  the  size  of  the  heart,  without  dropsy  and  with  no  marked  dyspnoea, 
and  this,  if  properly  appreciated,  will  be  found  to  throw  much  light  on  the 
nature  of  the  heart  disease,  and  to  indicate  the  line  of  treatment. 

§  176.  The  function  of  contractility The  circulation  is  carried  on 

by  the  force  derived  from  this  function  of  the  heart  muscle.  It  is  from 
this  source  that  the  arterial  pressure  is  maintained.  To  understand  the 
results  of  failure  or  exhaustion  of  this  function,  it  is  necessary  to  bear  in 
mind  certain  of  its  physiological  pecuharities.  After  each  contraction 
of  the  muscle-fibres  the  function  is  so  exhausted  that  no  further  contraction 
can  occur  until  a  brief  period  is  allowed  for  recovery.     If  the  stimulus  to 


192  DISEASES  OF  THE  HEART 

contract  is  applied  too  soon,  a  short  and  feeble  contraction  results.  If  a 
longer  period  of  rest  be  allowed,  the  contraction  will  be  longer  in  duration 
and  more  powerful,  so  that,  within  certain  limits,  the  longer  the  rest,  the 
longer  and  more  powerful  the  subsequent  contraction. 

Another  feature  to  keep  in  mind  when  considering  this  matter  is  that, 
like  aU  the  other  functions,  this  possesses  in  a  high  degree  the  peculiar 
property  of  '  reserve  force  '.  It  is,  in  a  measure,  the  too  easy  exhaustion 
of  the  reserve  force  which  is  the  subject  of  this  chapter. 

§  177.    Conditions    inducing    exhaustion    of    contractility These 

may  be  summed  up  in  the  general  statement  that  exhaustion  of  contractility 
occurs  when  the  heart  muscle  has  been  exposed  to  a  resistance  greater  than 
it  can  overcome  without  calling  upon  its  reserve  force.  This  may  be  brought 
about  by  the  healthy  heart  muscle  having  to  meet  abnormal  resistance, 
or  by  a  weakened  muscle  opposing  a  normal  resistance.  The  following 
description  includes  the  most  striking  of  these  conditions. 

(a)  Increased  frequency. — A  certain  rate  which  we  recognize  as  normal 
is  most  favourable  to  the  performance  of  the  heart's  work,  this  rate 
being  that  which  gives  time  for  the  functions  exhausted  by  the  contraction 
to  recover.  An  excessive  rate  prevents  the  due  recovery  of  the  function, 
and  a  call  is  made  upon  the  reserve  force,  which  thus  tends  to  become 
exhausted. 

(b)  Dilatation  of  the  heart. — A  certain  size  of  the  heart  is  also 
necessary  for  the  perfect  performance  of  contraction,  and  if  the  chambers 
be  dilated  the  contractile  force  is  placed  at  a  disadvantage,  and  exhaustion 
results. 

(c)  Obstruction  of  the  heart's  work. — Exhaustion  of  this  function  may 
arise  from  embarrassment  of  its  work  by  valvular  defects,  or  by  increased 
peripheral  resistance,  or  by  too  great  calls  made  upon  it  by  over-exertion. 

(d)  Imperfect  nutrition. — As  each  contraction  depends  on  the  supply 
of  appropriate  nutriment,  any  interference  with  this  leads  to  exhaustion. 
This  may  arise  from  deficient  supply,  on  account  of  the  small  output  of 
the  heart  (as  in  mitral  stenosis),  or  from  narrowing  of  the  coronary  arteries 
from  disease.  It  may  be  due  to  the  blood  containing  insufficient  nutriment 
of  the  special  kind  required,  or  containing  elements  that  have  a  deteriorating 
effect  on  the  muscle. 

(e)  Degeneration  of  the  muscle-fibres. — Finally,  there  may  be  changes  in  the 
heart  muscle  itself,  fibrous  or  fatty,  which  may  predispose  to  a  depression 
of  contractility  by  diminishing  the  number  of  the  fibres,  or  by  impairing 
the  activity  of  those  that  are  left. 

§  178.  Symptoms. — The    failure  of   this   function    may    occur    while 


EXHAUSTION  OF  CONTRA^CTILITY  193 

the  other  functions  of  the  heart  are  intact.  Thus  it  may  be  present  with 
the  heart  beating  at  a  normal  rate,  with  the  ventricular  systole  following 
normally  on  the  auricular,  and  with  the  heart  of  a  normal  size.  If  we 
analyse  the  symptoms  present  in  such  cases  where  the  other  functions  are 
intact,  we  can  then  refer  the  symptoms  with  a  fair  degree  of  certainty  to 
exhaustion  of  this  function. 

It  might  at  first  sight  be  supposed  that  failure  of  the  force  which  keeps 
up  the  arterial  pressure  would  show  itself  first  of  all  by  a  faU  in  arterial 
pressure.  This,  however,  is  not  the  case.  So  readily  does  the  heart  respond 
to  the  call  from  the  tissues  that  the  arterial  pressure  with  exhausted  con- 
tractility may  be  kept  up  to  an  extreme  height  until  the  moment  of  death. 
What  happens  first  is  an  exhaustion  of  the  reserve  force.  So  great  indeed 
may  the  exhaustion  be,  that  a  patient  may  be  scarcely  able  to  turn  over  in 
bed  without  distress,  and  yet  the  arterial  pressure  may  be  abnormally  high, 
and  the  size  of  the  heart  be  not  increased.  The  frequency  of  the  pulse 
and  respiration  may  be  normal  before  and  after  the  effort.  The  classes  of 
patient  where  the  failure  of  contractility  with  the  integrity  of  other  functions 
is  seen  most  strikingly  are  those  of  rheumatic  hearts  with  valvular  and 
myocardial  lesions,  and  those  of  cardio-sclerosis.  In  the  former  class  are 
the  young  and  middle-aged  who  have  had  rheumatic  fever  some  years 
before,  and  have  gone  on  doing  the  work  that  they  were  wont  to  do  when 
their  hearts  were  healthy.  Gradual  symptoms  of  exhaustion  appear  until 
they  become  so  clamant  that  exertion  has  to  be  restricted.  In  hke  manner, 
those  with  cardio-sclerosis  have  continued  their  wonted  exertion  until  pulled 
up  by  some  distressing  symptoms.  Exhausted  contractility  produces 
symptoms  in  a  twofold  manner,  {a)  by  reflexly  caUing  into  play  the  protective 
phenomena,  and  (&)  by  certain  changes  in  the  action  of  the  heart. 

(a)  Reflex  symytoms. — Concerning  the  first  of  these,  they  belong  to 
the  class  described  in  detail  in  Chapter  VII,  the  most  striking  being  the 
attacks  of  angina  pectoris.  Though  the  group  of  symptoms  included  in 
angina  pectoris  are  more  commonly  found  associated  with  exhausted  con- 
tractility in  cardio-sclerosis,  it  may  also  appear  in  the  young  with  mitral 
stenosis.  The  symptom  that  usually  arrests  the  patient  when  the  reserve 
contractile  force  is  exhausted  is  a  suffocating  feeling  coming  on  during  exer- 
tion, and  referred  to  the  throat  and  upper  part  of  the  chest,  or  breathless- 
ness,  or  a  sense  of  exhaustion.  Sometimes  it  is  a  distressing  consciousness 
of  the  heart  beat  (palpitation),  often  with  excessive  rapidity  of  the  heart. 
In  females  there  may  be  pain  complained  of  in  the  chest  and  left  arm,  and 
the  tissues  there  may  become  extremely  hyperalgesic. 

In  those  of  more  advanced  years  with  cardio-sclerosis,  the  symptoms 

MACEENZIB  Q 


194  DISEASES  OF  THE  HEART 

may  be  the  same,  though,  as  I  have  said,  angina  pectoris  is  far  more  frequent 
(see  Chapter  XXVII). 

(6)  Changes  in  the  heart's  action. — This  is  shown  by  the  pecuHar  irregu- 
larity— the  pulsus  alternans. 

§  179'  Pulsus  alternans. — A  very  striking  and  characteristic  sign  of 
exhausted  contractility  is  sometimes  seen  in  the  size  of  the  pulse  beat. 
I  have  repeatedly  dwelt  upon  the  fact  that  the  duration  and  force  of  con- 
traction depends  in  a  measure  on  the  length  of  the  preceding  period  of  rest. 
In  hearts  with  good  contractility,  recovery  after  a  contraction  is  so  rapid 
that  little  or  no  difference  can  be  detected  in  the  size  of  the  beat  after  pauses 
of  varying  duration.  In  cases  of  exhausted  contractility  the  matter  is 
very  different,  recovery  being  slow,  so  that  the  size  of  the  beat  has  a  distinct 
relation  to  the  length  of  the  preceding  diastolic  pause.  The  application  of 
this  law  assists  in  the  interpretation  of  many  obscure  conditions,  and  gives 
in  many  cases  a  clue  to  what  is  going  on  in  the  heart.  If  we  observe,  for 
instance,  what  happens  after  the  long  pause  following  on  an  extra-systole, 
we  find  a  different  reaction  in  different  hearts.  In  those  with  good  con- 
tractility, the  succeeding  beat  may  not  be  much  increased  in  size,  or  it  may 
be  big.  The  circumstances  causing  the  increased  size  are  complicated, 
such  as  the  greater  filling  of  the  heart  during  the  long  diastole,  the  lower 
arterial  pressure  which  the  contraction  has  to  overcome,  and  of  course  the 
longer  period  of  rest  for  the  restoration  of  the  contractility.  One  cannot, 
therefore,  draw  any  safe  deduction  from  the  character  of  the  first  beat  after 
the  long  pause.  But  the  second  and  third  beats  may  vary  remarkably. 
If  the  contractility  be  good  the  size  of  the  beats  after  the  first  big  beat  are 
uniform.  Sometimes,  however,  the  second  beat  is  smaller  than  the  third 
and  following  beats  (Fig.  125  a).  This  difference  in  the  size  of  the  beats  is 
a  very  important  one,  as  it  indicates  a  very  grave  exhaustion  of  contractility. 
Fig.  125  is  a  tracing  of  the  carotid  pulse  of  a  dog  whose  heart  was  dying 
from  exhaustion.  An  artificial  stimulus  applied  to  the  ventricle  produced 
the  extra-systole  r'.  The  next  beat  is  large,  and  is  followed  by  a  beat,  x , 
smaller  than  the  succeeding  beats.  A  very  similar  result  is  seen  in 
Figs.  125  a,  125  b,  and  126  from  patients  with  advanced  cardio-sclerosis. 
Not  infrequently,  the  difference  in  the  size  of  the  beats  persists  for  a  shorter 
or  longer  period,  in  such  a  manner  that  a  large  beat  alternates  with  a  smaller — 
the  pulsus  alternans  (Fig.  126).  F.  B.  Hoffman  ^^^  explained  this  alternating 
size  of  beats  in  the  frog's  heart  as  due  to  an  impairment  of  contractility, 
and  from  among  the  groups  of  allorhythmia,  where  every  second  beat 
rhythmically  varied,  Wenckebach  -^^  distinguished  one  where  a  small  beat 
regularly  followed  a  large  beat,  while  the  rate  of  the  heart  was  perfectly 


EXHAUSTION  OF  CONTRACTILITY  195 

regular.     He,  most  appropriately,  desires  to  limit  the  name  pulsus  alternans 
to  this  form  of  aUorhythmia.     Hitherto  the  name  has  been  applied  very 
loosely  to  arrhythmias  that  we  now  recognize  as  due  to  extra-systoles. 
The    explanation    of    the    cause    of    pulsus    alternans    is    as    follows  : — 


Fig.  125.  Tracing  from  the  carotid  artery  of  a  dog.  The  heart  was  exposed  and  the 
ventricle  directly  stimulated  to  produce  the  extra-systole  r'.  The  long  pause  after  the  extra- 
systole  is  followed  by  a  large  beat  and  succeeded  by  one  beat  (  X )  smaller  than  the  other  beats. 
Its  small  size  is  due  to  the  shorter  period  of  rest  preceding  it,  and  implies  grave  exhaustion  of 
the  contractile  power  of  the  left  ventricle.     Compare  with  Fig.  125  a  (Cushny). 

When  contractiUty  is  depressed,  if  time  be  allowed  for  a  full  and  strong 
contraction,  the  longer  duration  of  contraction  encroaches  upon  the  period 
of  rest,  so  that  by  the  time  the  next  stimulus  arrives  the  contractility  has 
not  sufficiently  recovered,  and  a  smaller  and  shorter  contraction  results. 


Fig.  125  a.  The  long  pause  after  the  extra-systole  (r')  is  followed  by  a  large  beat ;  this 
in  turn  is  followed  by  a  small  beat  (  x ),  and  the  succeeding  beats  are  larger.  The  small  beat  (  X ) 
is  an  evidence  that  the  contractility  of  the  heart  was  greatly  exhausted.  Compare  with 
Fig.  125.     (From  a  case  of  advanced  cardio-sclerosis.) 

As  this  contraction  is  shorter  in  duration,  the  period  of  rest  is  thereby 
lengthened  before  the  next  stimulus  arrives,  so  that  the  contraction  will 
be  stronger  and  longer  ;  being  longer  it  wiU  again  encroach  upon  the  period 
of  rest,  and  so  the  process  of  alternation  goes  on. 

o  2 


196  DISEASES  OF  THE  HEART 

This  variation  in  the  duration  of  the  systole  can  be  seen  in  Fig.  125  a 
by  noting  the  distance  between  the  up-stroke  and  the  dicrotic  notch  of  the 
radial  beats. 

I  have  now  collected  a  large  number  of  cases  in  which  this  irregularity 
occurs,  and  it  is  of  far  greater  frequency  than  is  usually  suspected.     The 


Fig.  125  b.    Shows  the  same  variation  as  Figs.  125  and  125  A.     (From  a  case  of  advanced 

fatty  and  sclerotic  heart.) 

condition  in  which  it  is  most  frequent  is  cardio-sclerosis,  where  it  is  usually 
associated  with  high  blood-pressure,  extra-systoles,  and  great  limitation  of 
the  field  of  cardiac  response,  and  not  infrequently  with  angina  pectoris 
(Cases  1  and  7,  see  Appendix  I).  After  a  period  of  rest  and  a  fall  of  arterial 
pressure,  it  may  entirely  disappear,  and  it  is  for  this  reason  that  it  is  so 
infrequent  in  hospitals,  where  the  rest  in  bed  favours  the  restoration  of 
the  contractility.  In  such  cases  I  have  frequently  been  able  to  bring  it 
back  by  making  the  patient  hurry  up  and  down  a  flight  of  stairs.  When 
it  is  associated  with  extra-systoles,  an  extreme  form  of  irregularity  may 
be  presented  which  seems  at  first  to  be  hopelessly  confused,  but  by  careful 
analysis  we  can  detect  the  extra-systole,  the  long  pause  after  it,  and  the 


^^^BBSB^^H^^^g2^^BSZ!B&&S8&8S&SS5S&&BHI 


Fig.  120.  The  alternating  character  of  the  pulse  is  increased  after  the  long  pause  following 
the  extra-systole  (r') ;  the  second  beat  (  X )  following  the  pause  appears  at  the  normal  interval, 
but  is  greatly  reduced  in  size.     (From  a  case  of  advanced  cardio-sclerosis.) 

marked  difference  in  the  size  of  the  following  beats  (see  Appendix  V). 
In  patients  who  have  exerted  themselves,  a  transient  but  extreme  irregularity 
may  sometimes  be  detected  in  the  pulse.  Small  beats  and  big  beats  may 
follow  one  another  in  a  bewildering  fashion.  But  so  brief  is  the  duration 
of  the  tumultuous  action  of  the  pulse,  that  before  one  can  apply  a  sphygmo- 


EXHAUSTION  OF  CONTRACTILITY  197 

graph  the  arrhythmia  has  to  a  great  extent  disappeared.  I  have,  how- 
ever, been  able  on  several  occasions  to  catch  the  irregularity  before  it  had 
subsided,  as  in  Figs.   127  and  128,  in  which  it  may  be  seen  how  variable 


Fig.  127.  This  tracing  and  the  next  were  taken  from  a  man  with  cardio-sclerosis,  after 
walking  up  a  steep  road.  The  pulse  felt  extremely  irregular,  and  an  analysis  of  the  tracing 
shows  it  to  have  been  regular  in  rhythm,  but  the  individual  beats  varied  greatly  in  force.  At  x 
the  exhaustion  is  so  great  that  only  a  small  wave  appears  in  the  radial. 

is  the  size  of  the  beats  ;  one  can  probably  infer  that  at  a:  a:  in  Fig.  128  the 
beats  were  too  weak  to  cause  a  movement  in  the  radial,  so  that  the  pulse  is 
intermittent  in  character. 


Fig.  128.  Intermittent  pulse  due  probably  to  extreme  exhaustion  of  contractility,  the 
contraction  of  the  ventricle  being  too  weak  to  send  a  wave  into  the  radial  artery  at  x.  Note 
the  increase  of  the  alternating  character  of  the  pulse  after  the  long  pause. 

It  may  appear  in  cases  of  cardio-sclerosis  after  an  exhausting  illness,  as 
bronchitis,  when  the  patient  is  confined  to  bed  (Fig.  129). 

I  have  found  this  pulsus  alternans  during  an  attack  of  paroxysmal 


Fig.  129.     Pulsus  alternans,  male,  64,  cardio-sclerosis  and  bronchitis. 

tachycardia  (Figs.  130,  and  228,  Appendix  III),  in  a  case  of  dilatation  of  the 
heart  from  some  obscure  cause,  in  acute  febrile  affections  of  the  heart  (pneu- 
monia and  rheumatic  fever),  and  after  the  administration  of  digitalis  (Figs. 
164  and  166). 


198 


DISEASES  OF  THE  HEART 


This  form  of  irregularity  must  be  distinguished  from  that  where  an 
extra-systole  alternates  with  a  normal  beat  (pulsus  bigeminus).  As  has 
already  been  described,  the  latter  form  of  irregularity  is  caused  by  the  too 


Fig.  130.     Pulsus  alternans  during  an  attack  of  paroxysmal  tachycardia,  sixty-six  hours 
from  its  commencement.     (Case  11,  Appendix  II.) 

early  appearance  of  the  smaller  beat,  which  is  followed  by  a  long  pause.  On 
the  other  hand,  the  rhythm  in  the  pulsus  alternans  is  quite  regular  (compare 
Figs.  131  and  132),  or  the  smaller  beat  occurs  after  a  slightly  lengthened 
pause.  Volhard  ^-^  has  pointed  out  that  this  slight  delay  is  due  to  the  fact 
that  the  weak  contraction  takes  a  longer  time  to  open  the  aortic  valves. 


Fig.  131.  Pulsus  bigemiuus,  due  to  the  regular  occurrence  of  extra- 
systoles.  The  numbers  represent  in  tenths  of  seconds  the  duration  of  each 
pulse  period,  and  it  is  seen  that  the  longest  pauses  occur  after  the  small 
beats.     (Compare  with  Fig.  132.) 

The  pulsus  alternans  can  sometimes  be  perceived  by  the  finger,  but  it 
is  apt  to  be  overlooked.  The  sounds  of  the  heart  often  can  be  heard  to 
alternate,  those  accompanying  the  weaker  being  less  loud.     When  there 


Fig.  132.     Pulsus  alternans.     The  numbers  show  a  slight  prolongation  of  the  pause  before 
the  smaller  beat,  in  contrast  to  what  occurs  in  Fig.  131. 

is  a  musical  murmur  the  alternation  in  the  strength  of  the  sounds  is  very 
marked  (Case  24,  Appendix  V). 

§  i8o.  Prognosis — The  prognosis  of  exhausted  contractility  naturally 
depends   on  the  conditions  that  have  induced  it.     These  conditions  are 


EXHAUSTION  OF  CONTRACTILITY 


199 


discussed  under  the  different  symptoms  described  elsewhere.  It  may, 
however,  be  pointed  out  that  the  pulsus  alternans  is  a  very  grave  sign  at  all 
times,  and  especially  in  febrile  affections.  In  cardio-sclerosis  it  implies  an 
advanced  degree  of  exhaustion,  and  one  may  confidently  infer  that  the 
muscular  degeneration  is  fairly  extensive,  as  I  have  found  in  a  number  of 
post-mortem  examinations.  A  patient  may  go  quietly  about  for  years 
after  the  appearance  of  the  pulsus  alternans,  but  it  is  usually  a  sign  of  an 
irrecoverable  underlying  condition. 


Fig.  133.     The  extra-systole  (?')  occurs  regularly  after  every  third  normal  beat.     The  two 
beats  preceding  the  extra-systole  are  of  equal  size  (22.  3.  '94). 

The  grave  significance  of  this  seemingly  trivial  sign  is  seen  in  the  case 
from  whom  Figs.  133  and  134  were  taken.  The  patient  was  a  female,  aged 
fifty,  whom  I  had  under  treatment  for  a  large  thoracic  aneurysm  about  ten 
years.  For  some  months  before  her  death  she  showed  extra-systoles  (Figs.  83 
and  84)  ;  on  March  22,  1894,  she  had  a  feverish  attack,  the  temperature 
102°,  and  the  pulse-rate  120,  still  showing  the  extra-systole  after  every  third 
normal  beat.  On  the  24th,  her  pulse-rate  and  irregularity  was  the  same 
(Fig.  134),  but  now  it  is  seen  that  the  second  beat  (  x  )  after  the  long  pause 


Fig.  134.  Shows  the  same  irregularity  as  Fig.  133,  but  here  the  second  of  the  normal  beats 
is  always  smaller  than  the  third,  implying  a  grave  exhaustion  of  the  contractile  power  of  the 
left  ventricle.     (Taken  24.  3.  '94.     The  patient  died  on  26.  3.  '94.) 

is  smaller  than  the  third.     She  died  on  March  26,  1894  (see  also  Case  7, 
Appendix  I,  and  Cases  23  and  24,  Appendix  V). 

§  1 8 1 .  Treatment. — While  the  treatment  will  depend  on  the  conditions 
causing  the  exhaustion,  we  can  obtain  from  the  pulsus  alternans  an  idea 
of  the  principle  which  should  guide  us  in  every  case.  Its  production  by 
excessive  work  in  degenerated  hearts,  or  after  a  long  period  of  tachycardia, 
implies  that  over-exertion  or  want  of  rest  is  the  immediate  cause.  The 
occurrence  of  the  larger  beat  in  the  alternating  pulse  shows  what  rest  can 
do  to  restore  the  contractility.     Therefore  relief  from  over-exertion,  whether 


200  DISEASES  OF  THE  HEART 

from  exercise,  rapid  action,  or  from  too  high  blood-pressure,  should  be  the 
aim.  This  may  be  secured  by  bodily  rest,  or  by  the  administration  of 
remedies  that  ensure  rest — above  all,  sleep.  When  there  is  a  high  blood- 
pressure,  dyspnoea,  and  no  dilatation  of  the  heart,  chloral  has  been  of  great 
use  in  my  hands.  On  the  other  hand,  drugs  of  the  digitalis  group  are  not 
only  useless,  but  may  be  injurious. 

In  a  few  cases  I  have  seen  distinct  relief  from  the  associated  symptoms 
of  pain  and  breathlessness  obtained  by  large  doses  of  oxygen  (p.  278). 


CHAPTER   XXIII 

Dilatation  of  the  Heart  (Failure  of  Tonicity) 

§  182.  The  cause  of  dilatation  of  the  heart. 

183.  The  function  of  tonicity. 

184.  The  symptoms  of  depression  of  tonicity. 

185.  Dilatation  of  the  heart. 

186.  The  cause  of  functional  murmurs. 

187.  The  consequences  of  dilatation  of  the  heart,  and  how  they  are  brought  about. 

188.  Dropsy. 

189.  Enlargement  of  the  liver. 

190.  Oedema  of  the  lungs. 

191.  Urinary  symptoms. 

192.  Prognosis. 

193.  Ti-eatment. 

Although  the  matter  of  the  '  tone  '  of  the  heart  is  frequently  present 
in  the  minds  of  physicians,  nevertheless  I  venture  to  doubt  if  ever  it  is  more 
than  a  vague  conception.  Some  writers  have  described  certain  conditions 
associated  with  it,  yet  it  has  not  received  that  consideration  its  importance 
merits.  The  recognition  of  depression  of  tonicity  will  be  found  to  be  of 
the  greatest  service  in  appreciating  the  nature  of  the  heart  failure  and  the 
remedies  appropriate  for  the  restoration  of  the  heart's  power.  For  some 
years  now,  I  have  been  inquiring  into  this  function,  and  although  many 
important  features  have  been  revealed,  I  am  far  from  comprehending  its 
full  significance. 

§  182.  The  cause  of  dilatation  of  the  heart. — Before  considering 
the  symptoms  produced  by  depression  of  tonicity,  it  is  necessary  to  appre- 
ciate the  cause  of  the  most  prominent  of  these  symptoms,  namely,  dilatation 
of  the  heart,  and  one  cannot  fail  to  be  struck  with  the  inadequacy  of  the 
explanation  usually  given  for  this  condition.  The  prevalent  idea  seems  to 
be  that  it  is  due  to  an  increasing  pressure  within  the  chambers  forcing  the 
walls  outwards.  But  if  it  be  asked,  Whence  comes  this  distending  force  ? 
the  inadequacy  of  such  an  explanation  is  at  once  apparent.  During  systole 
the  increased  pressure  within  the  chamber  is  produced  by  the  contraction 
of  the  wall  of  the  chamber  itself,  and  one  can  scarcely  assume  that  in  the 
process  of  contraction  dilatation  is  produced.     Dilatation  of  an  auricle, 


202  DISEASES  OF  THE  HEART 

it  is  true,  might  be  produced  by  the  forcible  regurgitation  of  blood  from 
a  powerful  ventricle,  but  such  a  thing  can  only  happen  when  there  is  a  lesion 
of  the  auriculo-ventricular  valves.  Regurgitation,  apart  from  valvular . 
lesion,  can  only  occur  after  the  muscle-fibres  surrounding  the  auriculo- 
ventricular  orifices  have  become  relaxed — that  is  to  say,  dilatation  of  the 
auricle  from  such  a  cause  would  be  produced  after  dilatation  of  the  ventricle. 

That  neither  the  resistance  opposed  to  a  chamber  during  the  systole, 
nor  the  distending  force  during  its  diastole,  is  the  cause  of  dilatation  becomes 
evident  when  the  conditions  observed  in  certain  hearts  are  carefully  studied. 
Thus  hearts  whose  walls  are  thinned,  and  whose  muscle-fibres  are  degenerated, 
may  continue  to  work  against  an  abnormally  high  arterial  pressure,  and 
never  show  any  signs  of  dilatation.  In  fact,  the  wall  of  the  left  ventricle 
may  be  so  thinned  that  it  actually  bursts  in  its  effort  to  overcome  the  aortic 
pressure,  yet  the  walls  show  no  signs  of  dilatation.  Professor  Keith,  who 
has  especially  looked  into  this  matter  of  ruptured  hearts,  informs  me  that 
such  hearts  may  show  no  sign  of  increase  in  the  size  of  their  cavities.  In 
a  patient  under  my  care  the  heart  was  so  enfeebled  that  he  could  scarcely 
walk  fifty  yards  without  an  attack  of  angina  pectoris  coming  on,  but  no 
enlargement  of  the  heart  could  be  detected.  He  died  suddenly  from  rupture 
of  the  heart,  and  I  found  that  part  of  the  heart-wall  was  so  thinned  as  to 
be  made  up  of  little  except  the  endocardium  and  pericardium,  yet,  notwith- 
standing this  enfeeblement  of  the  heart-waU,  there  was  no  sign  of  dilatation 
of  the  cavity. 

Dilatation  of  the  left  ventricle  may  occur  even  when  the  diastolic  force 
filling  the  ventricle  is  greatly  diminished,  as  in  cases  of  pure  mitral  stenosis. 
Here  the  quantity  of  blood  reaching  the  ventricle  and  the  force  with  which 
it  enters  the  ventricle  are  so  greatly  diminished  that  we  must  look  for  some 
other  cause  for  the  dilatation  of  the  left  ventricle  that  is  found  in  advanced 
cases  of  mitral  stenosis. 

§  183.  The  function  of  tonicity — In  default  of  this  mechanical 
explanation  we  turn  naturally  to  the  functions  of  the  normal  heart,  to  inquire 
what  maintains  the  fibres  in  health  in  a  position  short  of  their  extreme 
relaxation.  In  this  way  we  may  succeed  in  obtaining  a  more  definite  con- 
ception of  what  occurs  in  dilatation,  even  if  we  fail  to  elucidate  altogether 
its  etiology. 

This  function  of  maintaining  a  position  short  of  extreme  relaxation 
is  not  peculiar  to  the  cardiac  muscle,  but  is  also  met  with  in  the  ordinary 
skeletal  fibres,  and  in  both  cases  it  is  due  to  the  possession  by  the  fibres  of 
the  function  of  tonicity. 

§  184.  The  symptoms  of  depression  of  tonicity. — These  symptoms 


DILATATION  OF  THE  HEART  203 

are  threefold  :  (1)  those  due  directly  to  the  changes  in  the  heart,  viz. 
increased  size  of  the  heart,  alterations  in  the  position  and  in  the  character 
of  the  movements  of  the  heart,  and  the  presence  of  murmurs  ;  (2)  those 
associated  symptoms  due  to  the  failure  of  the  circulation  in  remote  organs 
and  tissues,  as  dropsy,  enlargement  of  the  liver,  and  breathlessness  ; 
(3)  certain  reflex  sensory  symptoms  mainly  shown  by  regions  of  hyperalgesia 
affecting  the  skin,  breast,  and  muscles  of  the  left  chest  and  axillary  fold,  and 
sometimes  also  the  left  sterno-mastoid  and  trapezius  muscles. 

§  185.  Dilatation  of  the  heart. — The  evidence  of  dilatation  of  the 
heart  is  made  out  by  marking  out  the  increased  size  of  the  heart.  I  need 
not  dwell  upon  how  this  is  done,  for  the  methods  for  percussing  out  the  heart's 
dullness  are  described  in  sufficient  fullness  in  every  handbook  of  physical 
diagnosis.  For  practical  purposes  the  transverse  dullness  at  the  level  of 
the  fourth  interspace  gives  on  the  whole  the  best  estimate  of  the  size  of  the 
heart.  In  exceptional  cases  the  whole  area  of  deep  dullness  may  be  with 
advantage  mapped  out,  as  when  dullness  is  found  extending  to  the  left 
above  the  third  rib.  In  such  cases  the  possibiHty  of  pericardial  effusion 
should  be  kept  in  mind. 

It  is  very  difficult  to  teU  with  certainty  what  share  each  chamber  of  the 
heart  takes  in  the  production  of  the  increased  size,  on  account  of  the  dis- 
placement of  the  whole  organ.  The  manner  in  which  the  heart  is  fixed 
above,  by  the  aorta,  pulmonary  artery  and  veins,  and  superior  vena  cava, 
and  below  by  the  inferior  vena  cava,  keeps  fixed  an  axis  on  which  the  heart 
to  a  certain  extent  rotates  in  the  enlargement  of  its  various  cavities.  The 
tendency  when  the  right  ventricle  dilates,  is  for  it  to  push  the  left  ventricle 
to  the  left  and  behind,  with  the  result  that  in  the  great  majority  of  cases 
we  get  evidence  of  an  extension  of  the  dullness  to  the  left.  When  the  right 
auricle  becomes  greatly  distended,  it  may  push  itself  to  the  front  of  the 
chest,  and,  as  Keith's  dissections  show,  compress  the  right  ventricle  to  a 
remarkable  degree.  When  there  is  extension  of  the  dullness  beyond  the 
right  border  of  the  sternum,  it  may  with  certainty  be  put  down  to  the  right 
auricle,  except  in  aneurysm  or  other  intra-thoracic  tumour. 

The  manner  in  which  the  right  heart  pushes  over  to  the  left  side  is  well 
brought  out  in  Figs.  135  and  136.  These  are  typical  of  the  dilatation 
secondary  to  mitral  stenosis.  If  a  comparison  be  made  with  the  position 
of  the  chambers  in  the  normal  heart  (Fig.  19),  it  will  be  observed  that  the 
increase  to  the  right  side,  notwithstanding  the  great  dilatation  of  the  right 
heart,  is  very  sHght,  whereas  the  great  increase  in  the  size  of  the  heart  is 
to  the  left — sometimes  with  only  a  slight  depression  of  the  apex  (Fig.  135), 
sometimes  with  considerable  depression   (Fig.    136).     Note  also  how  the 


204 


DISEASES  OF  THE  HEART 


right  auricle  pushes  into  the  second  left  interspace.  So  long  as  the  lungs 
cover  a  portion  of  the  heart  the  perceptible  movements  will  be  entirely  due 
to  the  right  ventricle  ;  but  when  the  lung  is  pushed  from  the  front  of  the 
heart,  then  the  real  apex  will  be  found  at  the  extreme  left  (see  §  83). 

In  seeking  for  the  cause  of  the  increased  dullness,  the  character  of  the 
impulse  should  always  be  studied,  not  only  to  determine  the  nature  of  the 


Fig.  135.  Position  of  the  chambers  of  the  heart  in  extreme  dilatation,  as  in  the  late  stage 
of  mitral  stenosis.  The  portion  of  the  heart  on  the  right  of  the  sternum  shaded  deeply- 
together  with  that  behind  the  sternum  up  to  the  dotted  line  represents  the  right  auricle,  while 
the  small  strip  to  the  left  shaded  deeply  represents  the  left  ventricle.  The  part  between  is 
the  right  ventricle.     (Harris). 

heart's  enlargement,  but  to  distinguish  it  from  pericardial  effusions  and 
displacement  of  the  heart  by  such  conditions  as  aneurysm,  pleural  effusion, 
and  so  forth.  Another  point  to  bear  in  mind  is  that,  in  the  early  stages  of 
enlargement  of  the  heart,  the  lung  may  still  cover  a  part  of  its  left  border, 
but  with  persistence  of  the  enlargement  the  lung  is  compressed,  and  if  non- 
adherent, recedes  from  the  anterior  surface  of  the  heart,  altering  altogether 
the  character  of  the  apex  movements. 

§  1 86.    The  cause  of    functional   murmurs — Functional  murmurs 


DILATATION  OF  THE  HEART  205 

have  hitherto  been  looked  upon  as  a  consequence  of  simple  dilatation  of  the 
heart,  but  this  explanation  is  far  from  being  sufficient.  Thus  we  may  have 
considerable  dilatation  of  the  heart  without  a  murmur.  Again,  we  may 
have  very  little  dilatation  with  marked  systolic  murmurs  at  apex  and  base, 
and  with  a  great  regurgitant  wave  in  the  veins.  The  explanation  of  these 
apparent  anomalies  seems  to  be  in  the  condition  of  the  muscles  supporting 


Fig.  136.    Dilatation  of  the  heart  with  the  apex  beat  displaced  downwards.     The 
shading  is  the  same  as  in  the  preceding  figure. 

the  auriculo-ventricular  orifice.     If  their  tonicity  be  depressed  regurgitation 
ensues,  and  gives  rise  to  the  functional  murmurs. 

§  187.  The  consequences  of  dilatation  of  the  heart,  and  how  they 
are  brought  about — Before  describing  in  detail  the  results  that  foUow 
dilatation  of  the  heart,  it  is  necessary  to  consider  the  manner  in  which 
these  symptoms  of  heart  failure  are  brought  about.  The  maintenance 
of  the  circulation  is  due  to  the  contractile  force  of  the  heart,  and  normally 
the  factors  concerned  are  so  balanced  that  everything  is  done  to  facilitate 


206  DISEASES  OF  THE  HEART 

the  work  of  the  heart.  It  is  reasonable  to  assume  that  the  chambers  of  the 
heart  are  normally  of  the  size  that  enables  them  to  contract  with  the  greatest 
efficiency.  The  dilatation  of  these  chambers  will  therefore  embarrass  the 
heart  muscle,  with  the  usual  result,  a  limitation  of  the  reserve  force.  At 
first,  this  limitation  may  only  call  forth  disagreeable  symptoms  when  it  is 
exhausted,  the  exhaustion  occurring  much  sooner  than  normal.  The 
degree  of  exhaustion  depends  on  the  integrity  of  the  heart  muscle.  If  the 
contractile  force  is  embarrassed  by  inherent  defects  of  the  muscular  wall, 
or  by  other  causes,  such  as  irregularity  of  action,  or  valvular  defects,  then 
the  heart  failure  corresponds  to  the  degree  of  embarrassment  and  inability 
of  the  muscle  to  overcome  it.  For  this  reason  we  find  all  degrees  of  heart 
failure  associated  with  dilatation.  In  the  milder  cases  there  may  be  only 
the  subjective  symptoms  of  breathlessness,  palpitation,  and  weakness.  In 
the  more  extreme  cases,  dropsy  (more  or  less  extensive),  diminished  secretion 
of  urine,  effusion  of  fluid  into  the  serous  cavities,  enlargement  of  the  liver, 
lividity  of  the  face  may  be  present.  The  rationale  of  the  production  of  this 
extreme  heart  failure  seems  to  be  as  follows  :  So  long  as  the  contractile 
force  of  the  heart  is  able  to  maintain  a  degree  of  arterial  pressure  sufficient 
to  supply  the  organs  and  tissues,  the  heart  failure  will  be  limited  to  those 
subjective  symptoms  involved  in  a  great  reduction  of  reserve  force  ;  the 
patient  is  comfortable  at  rest,  for  the  heart  is  then  able  to  maintain  the 
circulation,  but  is  distressed  by  exertion,  for  the  heart  has  so  Httle  reserve 
force  that  it  is  unable  to  meet  the  extra  demand.  When  the  force  of  the  heart 
fails  to  maintain  the  arterial  pressure  at  the  height  necessary  for  the  tissues, 
then  we  get  the  symptoms  in  the  remote  organs  and  tissues  (dropsy,  ascites, 
enlarged  liver,  &c.). 

I  have  endeavoured  in  a  number  of  ways  to  demonstrate  the  relationship 
between  dilatation  of  the  heart  and  these  evidences  of  extreme  heart  failure, 
and  I  give  a  few  instances  where  the  association  of  these  symptoms  with 
dilatation  of  the  heart  is  clearly  marked. 

In  advanced  cases  of  cardio-sclerosis  with  a  blood-pressure  continuously 
high,  between  180  mm.  Hg.  and  200  mm.  Hg.,  the  heart  may  be  of  normal 
size,  or  only  very  slightly  enlarged.  There  is  great  limitation  of  the  field 
of  response,  exertion  readily  inducing  attacks  of  angina  pectoris  or  breath- 
lessness, Cheyne-Stokes  respiration  may  occur  also,  and  attacks  of  cardiac 
asthma  or  severe  dyspnoea  at  nights.  There  may  be  large  pulsation  in  the 
veins  of  the  neck,  but  no  dropsy.  Patients  may  gradually  weaken  and  die, 
and  the  heart  remain  unchanged  in  size.  On  the  other  hand,  in  the  course 
of  a  day  or  two,  one  may  be  struck  by  a  great  change.  The  patient  seems 
easier  ;  the  blood-pressure  has  fallen  to  150  mm.,  or  lower  ;  attacks  of  angina 


DILATATION  OF  THE   HEART  207 

pectoris,  cardiac  asthma,  and  Cheyne-Stokes  respiration  disappear.  But 
the  legs  begin  to  swell,  the  urine  becomes  scanty,  the  jugular  pulse  disappears, 
the  breathing  is  continuously  hurried,  and  the  patient  has  to  be  propped  up 
in  bed.  He  may  begin  to  expectorate  blood-stained  mucus,  and  there  is 
evidence  of  oedema  of  the  base  of  the  lung.  If  the  heart  be  examined,  it 
will  be  found  to  extend  one  or  two  inches  further  to  the  left,  and  it  may  be 
a  mitral  murmur  has  developed. 

Even  more  striking,  because  more  sudden  and  violent,  are  the  changes 
that  take  place  in  certain  cases  of  paroxysmal  tachycardia.  In  describing 
this  condition  (Chapter  XX),  I  pointed  out  that  the  symptoms  varied  in 
patients  according  to  the  condition  of  tonicity, — if  the  heart  remained 
unaltered  in  size  during  an  attack,  the  symptoms  were  less  marked,  and  the 
condition  less  grave  than  if  the  heart  dilated.  In  the  cases  recorded  in  the 
Appendix  (Cases  11  and  12,  Appendix  II),  the  heart  dilated,  and  in  the  course 
of  a  few  hours  symptoms  of  extreme  heart  failure  set  in.  I  have  seen  these 
cases  on  several  occasions  shortly  before  an  attack,  and  watched  the  steady 
progress  of  the  change.  The  hearts  were  nearly  normal  in  size,  but  in  three 
hours'  time  the  transverse  diameter  had  increased  by  two  inches,  the  face 
had  become  livid  and  the  lips  swollen.  The  veins  of  the  neck,  which  had  shown 
little  movement,  now  pulsated  largely  in  the  nodal  rhythm.  In  the  course 
of  twenty-four  hours  oedema  of  the  legs  appeared,  and  the  liver  became  large, 
and  in  one  case  pulsated.  After  some  days  the  dropsy  extended  up  the 
legs,  the  abdomen  became  distended,  and  the  urine  scanty.  With  the 
cessation  of  the  attack  of  paroxysmal  tachycardia,  the  patients  at  once 
experienced  relief,  and  in  a  few  hours  every  vestige  of  heart  failure  had 
disappeared,  and  the  heart  itself  returned  to  a  normal  size  and  rhythm. 
I  give  these  instances  because,  owing  to  the  sudden  change  of  appearance, 
one  could  account  fairly  satisfactorily  for  the  symptoms.  In  various  modi- 
fications they  will  be  found  associated  with  extreme  heart  failure  from  all 
forms  of  cardiac  disease.  I  have  seen  many  cases  in  which  the  inception 
of  the  nodal  rhythm  was  followed  by  these  changes,  and  when  it  persisted 
a  partial  recovery  only  followed,  with  reduction  of  the  size  of  the  heart.  In 
certain  alcoholic  hearts — especially  in  those  of  Graham  Steell's  group  of 
'  muscle  failure  ' — these  phenomena  can  also  be  recognized,  as  well  as  in 
other  conditions. 

This  manner  of  looking  at  dilatation,  and  the  cause  of  dropsy  and  other 
symptoms,  has  a  very  practical  bearing  on  the  treatment  of  heart  failure 
associated  with  valvular  disease,  the  nodal  rhythm,  and  cardio-sclerosis. 

§  1 88.  Dropsy Oedema  of   the  subcutaneous  tissues  is   a   common 

feature  in  heart  failure  with  dilatation.    It  is  apart  from  my  purpose  to 


208  DISEASES  OF  THE  HEART 

discuss  the  various  theories  propounded  to  account  for  its  occurrence,  it  being 
sufficient  here  to  note  that  its  appearance  is  often  a  definite  sign  of  heart 
dilatation,  and  its  disappearance  an  equally  definite  sign  of  restoration  of 
the  heart's  tone.  It  begins  first  in  the  most  dependent  parts  :  in  people  not 
confined  to  bed  it  is  found  first  about  and  above  the  ankles  ;  in  people  lying 
in  bed,  across  the  sacrum.  It  may  linger  in  the  legs  for  years  in  some  folks — 
worse  towards  night,  better  in  the  morning.  In  extreme  cases  it  invades  the 
thighs  and  abdominal  waU.  The  loose  cellular  tissue  of  the  scrotum  and  the 
penis  and  vulva  becomes  infiltrated,  and  may  attain  an  enormous  size.  Before 
marked  effusion  takes  place  into  the  abdominal  cavity,  the  bowels  often 
become  greatly  distended.  It  may  finally  invade  the  pleural  cavities, 
producing  hydrothorax.  The  distended  abdomen  and  the  hydrothorax 
add  to  the  embarrassment  of  the  breathing.  If  the  patient  leans  more  to 
one  side  than  to  the  other,  in  extreme  cases,  the  arm  and  check  of  that  side 
may  become  greatly  swollen.  When  an  arm  becomes  swollen  apart  from 
this,  and  where  there  is  not  extensive  oedema,  one  may  suspect  a  clot  in 
some  of  the  larger  veins  in  or  near  the  chest. 

Associated  with  dropsy  there  is  usually  a  diminished  urinary  secretion, 
and  disappearance  of  the  dropsy  usually  coincides  with  an  increased  flow 
of  urine. 

The  significance  of  oedema  is  extremely  varied.  Many  elderly  people, 
especially  if  they  are  stout,  may  for  years  have  their  legs  more  or  less  swoUen 
even  if  their  hearts  present  no  particular  abnormahty  beyond  a  shght  dilata- 
tion, though  it  is  more  common  amongst  those  with  the  nodal  rhythm.  It  may 
be  present  in  attacks  of  heart  failure  to  an  extreme  degree,  with  ascites  and 
hydrothorax,  and  notwithstanding  the  patient  may  make  a  good  and  lasting 
recovery.  These  are  found  more  particularly  in  cases  of  rheumatic  affection 
of  the  heart  of  some  duration,  starting  in  some  with  the  nodal  rhythm. 
If  the  heart  reverts  to  its  normal  rhythm,  the  disappearance  of  the  dropsy 
is  more  speedy  than  its  onset.  If  the  heart  reacts  to  digitalis,  the  disap- 
pearance of  the  dropsy  accompanies  the  other  beneficial  effects  of  the  drug. 
When  all  attempts  to  restore  the  heart  fail,  the  dropsy  increases,  embarrasses 
the  heart  and  the  respiration  by  effusion  into  the  serous  cavities,  and  adds 
much  to  the  suffering  of  the  patient,  who  drifts  to  a  fatal  issue. 

§  189.  Enlargement  of  the  liver Another  result  of   the  failure    of 

the  circulation  secondary  to  dilatation  of  the  heart  is  sweUing  of  the  hver 
from  passive  congestion  (Chapter  XIV).  It  may  not  appear  in  the  earher 
stages  in  the  first  instance,  but  when  a  patient  has  once  recovered  from 
an  attack  of  heart  failure  with  enlargement  of  the  hver,  every  subsequent 
attack  induces  this  symptom,  sometimes  before  any  sign  of  dropsy  sets  in. 


DILATATION  OF  THE  HEART  209 

There  may  be  associated  with  the  enlargement  a  certain  amount  of 
jaundice,  and  the  combination  of  enlarged  Uver  and  jaundice,  with  the  wasting 
that  sometimes  accompanies  long-continued  heart  failure,  may  raise  the 
suspicion  of  mahgnant  disease  of  the  liver  (§  121).  The  dilatation  or 
irregular  action  of  the  heart  should  direct  attention  to  the  real  nature  of 
the  trouble. 

There  may  be  a  considerable  degree  of  pain  and  discomfort  associated 
with  the  enlargement  of  the  liver,  and  the  painful  contracted  muscles  may 
embarrass  the  respiration  (described  in  §  117). 

§  190.  Oedema  of  the  lungs. — A  symptom  of  great  value  is  found  in 
the  careful  auscultation  of  the  bases  of  the  lungs  in  cases  threatened  with 
some  forms  of  heart  failure.  I  carried  out  for  some  years  an  extensive 
observation  on  all  kinds  of  people — healthy,  and  with  failing  hearts  from 
a  great  variety  of  causes — and  I  was  able  to  anticipate  attacks  of  heart 
failure  in  a  great  number  of  cases.  If  one  systematically  examines  the 
bases  of  the  lungs  in  elderly  people  who  are  perforce  confined  to  bed,  as  in 
consequence  of  an  operation  or  a  fractured  leg,  in  a  certain  proportion  the 
earliest  symptom  of  heart  failure  wdll  be  found  in  the  appearance  of  fine 
crepitations  at  the  bases  of  the  lung.  The  same  experience  will  be  met  with 
in  patients  confined  to  bed  from  any  exhausting  complaint,  particularly  if 
the  heart  muscle  be  involved  in  the  ailment,  as  in  typhoid  fever.  Many 
patients  with  mitral  lesions  have  no  dropsy,  but  suffer  from  severe  attacks 
of  heart  failure  with  great  breathlessness.  In  such  cases  the  bases  of  the 
lungs  will  be  found  to  show  signs  of  oedema  at  the  early  stages  of  the  break- 
down. 

It  has  been  my  habit  in  these  cases  to  begin  the  examination  of  the  patient 
by  asking  him  on  which  side  he  lies,  then  make  him  sit  up,  and  while  I  auscul- 
tate the  base  of  that  lung  on  the  side  he  had  lain,  I  ask  him  to  take  in  one  full 
and  deep  inspiration.  This  opens  up  the  alveoli  at  the  base,  and  if  there  is 
any  abnormal  moisture  it  is  manifested  by  numerous  fine  crepitations. 
Healthy  people  show  no  sign  of  this.  Slightly  weakened  hearts  may  show 
it  with  the  first  deep  inspiration  only  ;  if  there  is  distinct  cardiac  enfeeblement 
the  crepitations  do  not  disappear  at  first,  but  persist.  I  have  seen  cases 
where  the  first  sign  was  the  crepitation  during  the  first  deep  inspiration,  and 
gradually  the  crepitations  became  more  persistent  until  the  resonance  of  the 
bases  of  the  lung  became  impaired,  even  to  complete  dullness,  with  no  breath 
sounds,  and  at  the  post-mortem  examination  the  lungs  at  the  bases  have 
been  sodden  and  airless.  In  some  instances  there  have  been  patches  of  in- 
flammation (catarrhal  pneumonia — the  hypostatic  pneumonia  of  the  feeble). 

MACKENZIE  p 


210  DISEASES  OF  THE  HEART 

I  have  also  seen  this  hjrpostatic  congestion  disappear,  and  as  the  patient 
improved  the  crepitations  gradually  disappeared,  the  last  sign  being  the 
crepitations  with  the  first  deep  inspiration. 

I  have  found  this  method  of  observation  of  the  greatest  practical  use. 
In  the  elderly  it  governs  the  position  which  the  patient  should  occupy — 
lying  down  or  propped  up.  In  typhoid  fever  it  is  a  prognostic  sign  of  the 
very  greatest  value — the  absence  of  oedema  indicating  that  the  heart  has 
escaped  infection  ;  its  presence  and  gradual  increase,  a  sign  of  great  gravity. 
In  heart  disease  it  is  likewise  one  indication  of  the  heart's  condition,  and  in 
the  compHcation  of  pregnancy  and  heart  disease  it  is  one  of  the  most 
important  guides  in  the  management  of  these  cases. 

It  is  of  no  less  importance  in  treatment,  as  will  be  realized  when  the 
reason  for  its  appearance  is  appreciated.  It  invariably  accompanies  dila- 
tation of  the  right  heart,  and  the  manner  of  its  production  is  as  follows  :  The 
factors  that  move  the  blood  through  the  lungs  are  twofold — first  and  most 
important,  the  right  ventricle  ;  and  second,  the  movements  of  respiration. 
In  healthy  hearts  the  first  of  these  is  so  powerful  that  the  second  is  scarcely 
appreciated.  When,  however,  the  right  ventricle  is  enfeebled,  the  assistance 
of  the  respiratory  movements  becomes  necessary.  When  the  patient  lies 
in  bed  on  one  side,  the  pressure  of  the  ribs  on  the  mattress  restrains  their 
movement,  so  that  the  flow  of  blood  through  this  part  of  the  lung  is  retarded, 
and  oedema  results.  This  can  be  shown  in  the  early  stages,  for  when  the 
patient  breathes  deeply  the  whole  of  the  crepitations  may  disappear. 

From  this  account  will  be  realized  the  part  that  can  be  played  in  suit- 
able cases  by  placing  the  patient  in  a  position  to  breathe  freely,  avoiding 
the  restraint  exerted  by  pressure  on  the  ribs,  and  by  making  the  patient 
deeply  inspire.  In  addition,  the  importance  of  recognizing  the  nature  of 
the  symptoms  due  to  the  enlargement  of  the  liver  is  here  apparent,  where 
not  only  the  abdominal  muscles,  but  the  intercostals  also,  may  be  tender 
and  contracted.  In  thus  ceasing  to  act  as  respiratory  agents,  while  exer- 
cising their  primitive  function  of  protection,  these  contracted  muscles 
further  add  to  the  embarrassment  of  the  heart  in  its  work. 

§  191.  Urinary  symptoms — I  doubt  if  ever  we  get  the  characteristic 
urinary  symptoms  of  heart  failure  in  the  absence  of  dilatation  of  the  heart. 
These  symptoms  are  a  scanty  secretion  and  increased  specific  gravity,  and 
frequently  the  presence  of  albumen.  A  diminished  supply  of  blood  to  the 
kidneys  may  cause  a  large  quantity  of  albumen  to  appear  in  the  scanty 
urine,  as  can  be  observed  in  heart-block  and  nodal  bradycardia,  when  the 
heart's  rate  becomes  very  infrequent.  The  diminution  of  the  quantity 
usually  goes  hand  in  hand  with  the  dropsy.      The  cause  in  the  main  is 


DILATATION  OF  THE  HEART  211 

a  fall  in  arterial  pressure  and  a  rise  in  the  venous,  with  consequent  venous 
stasis  in  the  kidneys.  Other  conditions  may  co-operate,  such  as  the  chemical 
constitution  of  the  fluid  in  the  tissues  and  changes  in  the  secreting  cells  of 
the  kidney.  It  is  often  a  difficult  point  to  determine  whether  the  albu- 
minuria has  been  pre-existent,  or  whether  it  is  induced  by  the  venous  stasis 
and  subsequent  inflammatory  changes  in  the  kidneys.  The  history  of  the 
patient  will  help,  and  the  presence  of  arterio-sclerosis  and  retinitis  point  to 
a  pre-existent  Bright's  disease.  It  may  be  necessary  to  suspend  judgement 
until  a  recovery  of  tonicity  of  the  heart  restores  the  circulation,  as  with  the 
increase  in  flow  of  urine  the  albuminuria  may  entirely  disappear. 

It  is  often  useful  to  direct  the  patient's  attention  to  the  urinary  secretion, 
as  its  diminution  may  give  the  first  warning  of  an  impending  breakdown, 
and  the  increase  in  the  flow  is  often  the  first  sign  of  recovery  of  heart 
power. 

§  192.  Prognosis. — While  the  degree  of  tone  present  is  of  first-class 
importance  in  estimating  the  nature  of  the  heart  failure,  we  must  use  great 
discretion  in  determining  the  value  of  dilatation  as  a  prognostic  factor. 
Great  dilatation  may  be  compatible  with  a  favourable  prognosis,  while 
a  much  smaller  degree  of  dilatation  may  be  a  sign  of  considerable  gravity. 
If  we  find  the  patient  getting  along  comfortably  and  well  with  a  dilated  heart, 
it  means  that  the  muscular  tissue  is  otherwise  sound,  and  that  there  is  no 
material  obstacle  to  the  work  of  the  heart,  and  the  muscle  itself  is  able  to 
overcome  the  embarrassment  induced  by  the  dilatation. 

Another  element  in  the  prognosis  is  the  manner  in  which  the  heart 
responds  to  treatment,  especially  to  drugs  of  the  digitalis  group.  As  I  shall 
point  out  in  Chapter  XXXIV,  tonicity  is  one  of  the  functions  of  the  heart 
which  digitalis  readily  affects  in  many  cases,  and  it  is  probably  because  of 
the  effects  of  this  drug  on  this  function  that  it  has  often  such  a  wonderfully 
beneficial  infiuence  on  the  heart.  The  improvement  produced  by  digitalis 
is  therefore  a  guide  to  the  condition  of  the  heart  muscle,  and  to  the  suscepti- 
bility of  this  function  to  its  action.  On  the  other  hand,  when  dilatation 
of  the  heart  and  the  symptoms  accompanying  it  described  above  are 
unresponsive  to  digitahs,  the  outlook  becomes  grave.  Especially  is  this 
the  case  in  the  heart  failure  with  dilatation  in  advanced  arterio-sclerosis. 

§  193.  Treatment — As  dilatation  is  invariably  secondary  to  some 
other  condition  of  the  heart,  the  treatment  has  to  take  into  considera- 
tion other  factors.  I  may  point  out,  however,  that,  unless  in  the  acute 
febrile  stage,  dilatation  is  an  indication  for  the  prescription  of  digitahs  in 
all  rheumatic  hearts.     In  other  conditions  it  should  be  tried,  especially  if 

there  is  dropsy  and  deficient  secretion  of  urine.     The  treatment  of  such 

p  2 


212  DISEASES  OF  THE  HEART 

associated  symptoms  as  dropsy  and  diminution  of  urine  should  consist  in  the 
attempt  to  restore  the  heart's  strength.  When  dropsy  becomes  a  distressing 
symptom,  special  means  have  to  be  undertaken  for  its  removal.  As  free 
diuresis  is  the  most  effective  way  of  getting  rid  of  it,  a  great  many  agents  are 
recommended  which  effect  this  purpose.  The  virtues  of  many  a  prescription 
can  be  estabhshed  by  the  recital  of  illustrative  cases  in  which  its  exhibition 
was  followed  by  an  extraordinary  discharge  of  urine  and  speedy  disappear- 
ance of  all  dropsy.  These  preparations  will  be  found  to  vary  from  the 
mixtures  containing  every  conceivable  drug  that  is  supposed  to  have  diuretic 
properties,  to  some  recent  synthetical  preparation.  The  fact  of  the  matter 
is,  that  in  many  of  these  cases  the  secretory  activity  of  the  kidneys  seems 
to  be  in  temporary  abeyance,  and  some  sUght  adventitious  aid  gives  it  the 
necessary  stimulus.  This  auspicious  moment  coinciding  with  the  adminis- 
tration of  the  drug,  results  in  a  profuse  diuresis.  This  aid  need  not  be  a  drug. 
I  have  seen  a  patient,  who  had  to  sit  up  in  a  chair  for  three  weeks  on  account 
of  his  breathing,  become  extremely  dropsical,  passing  very  little  urine. 
The  mere  return  to  bed  was  followed  at  once  by  a  profuse  diuresis  and  the 
rapid  disappearance  of  the  dropsy.  It  is,  however,  necessary  in  many  cases 
to  try  various  agents,  and  happily  here  the  digitalis  group  is  most  effective, 
the  combination  of  digitalis,  squill,  and  calomel  being  particularly  useful, 
not  only  from  its  action  on  the  heart  and  kidneys,  but  also  from  its  effects 
on  the  bowels.  When  these  drugs  fail  others  may  be  found  to  act,  such  as 
theobrominae  sodii  saHcylas  (Diuretin)  or  theocin-sodium  acetate.  In 
some  cases  the  elimination  of  common  salt  from  the  food  helps  to  reduce 
the  dropsy.  In  all  cases  of  dropsy  the  bowels  should  invariably  be  kept 
well  moved. 

Special  efforts  to  give  relief  are  often  necessary.  In  certain  cases  when 
the  patient  can  go  about,  an  elastic  bandage  skilfully  appUed  is  beneficial, 
particularly  in  those  hard,  swollen  legs  when  the  skin  threatens  to  give  way. 
Massage  also  is  of  assistance.  When  the  legs  or  genitals  become  greatly 
distended,  deep  pricks  with  a  needle  will  often  be  followed  by  a  free  flow 
of  serum  and  a  great  diminution  of  the  swelling.  The  utmost  cleanliness 
should  be  observed  in  carrying  out  this  simple  procedure.  The  employment 
of  Southey's  tubes  inserted  into  the  legs  or  abdominal  cavity  will  often 
drain  off  a  large  quantity  of  fluid.  The  abdominal  and  thoracic  cavities 
may  need  to  be  tapped  ;  such  tapping  invariably  gives  temporary  relief. 
In  some  advanced  cases  where  the  penis  is  greatly  swollen  (ram's  horn), 
there  may  be  inability  to  void  urine.  In  using  a  catheter  there  may  be 
some  trouble  in  finding  the  meatus,  the  glans  penis  being  buried  in  the 
scrotum  under  the  swollen  prepuce.     If  the  swollen  foreskin  be  gently  but 


DILATATION  OF  THE  HEART  213 

firmly  grasped  in  the  hand  and  compressed,  the  fluid  is  driven  out,  and 
the  glans  can  then  be  exposed. 

The  employment  of  judicious  breathing  exercises  in  oedema  of  the  lung 
is  often  beneficial,  the  patient  sitting  up  and  breathing  slowly  and  deeply. 
In  severe  cases  this  is  limited  at  first  to  a  few  movements.  If  the  patient 
bears  the  exercise,  these  deep  respirations  should  be  employed  at  regular 
intervals  every  two  or  three  hours  when  awake.  In  the  intervals  the 
patient  should  be  propped  as  high  as  he  can  bear  with  comfort. 


CHAPTER  XXIV 

Acute  Febrile  Affections  of  the  Heart 

§  194.  INIanner  in  which  the  heart  is  affected  in  fever. 

195.  The  febrile  heart. 

196.  Acute  febrile  affections  of  the  heart. 

197.  Symptoms  in  myocarditis :    changes  in  rate,  changes  in  rhythm  due  to  depressed 

conductivity  of    the    a. -v.   bundle,   depressed    contractility,   extra-systole,  nodal 
rhythm,  depressed  tonicity  (dilatation  of  the  heart). 

198.  Symptoms  in  endocarditis. 

199.  Symptoms  in  pericarditis. 

200.  The  heart  in  rheumatic  fever  :    pathological  changes,  symptoms. 

201.  The  heart  in  pneumonia. 

202.  The  heart  in  diphtheria. 

203.  The  heart  in  septic  iijfections. 

204.  Treatment.     • 

§  194.  Manner  in  which  the  heart  is  affected  in  fever. — In  con- 
sidering the  state  of  the  circulation  in  febrile  conditions,  it  is  necessary 
to  bear  in  mind  three  facts,  viz.  that  the  heart's  action  is  modified  by  an 
increase  in  temperature,  that  the  heart  reacts  differently  according  to  the 
toxins  produced  by  the  agent  causing  the  fever,  and  finally,  that  the  heart 
itself  may  be  the  seat  of  the  conditions  causing  the  fever.  Recent  researches 
demonstrate  conclusively  the  invasion  of  the  heart  by  the  specific  organism  in 
rheumatic  fever,  pneumonia,  typhoid  fever,  diphtheria,  erysipelas,  influenza, 
and  various  septic  infections.  The  results  of  such  invasion  are  shown  in 
the  occurrence  of  endocarditis,  myocarditis,  and  pericarditis.  The  symp- 
toms evoked  in  such  invasions  are  not  always  distinctive,  and  may  resemble 
the  symptoms  induced  in  the  heart  by  febrile  conditions  alone,  or  by  toxins 
produced  from  other  sources  in  the  body.  I  dwell  upon  this  because  an 
attempt  should  always  be  made  in  febrile  conditions  to  judge  rightly  the 
effects  on  the  heart.  One  cannot  but  be  struck,  for  instance,  by  the  fact 
that  people  with  previously  seriously  damaged  hearts  may  pass  scatheless 
through  severe  attacks  of  pneumonia  or  typhoid  fever,  while  the  young 
and  vigorous  may  succumb  after  a  few  days'  illness  on  account  of  the 
implication  of  the  heart  in  the  disease. 

Another  point  to  bear  in  mind  is  that  in  the  invasion  of  the  heart  the 
specific  organism  rarely  affects  one  tissue  alone.     In  order  to  be  exact  and 


ACUTE  FEBRILE  AFFECTIONS  OF  THE  HEART  215 

methodical,  writers  usually  describe  separately  the  symptoms  of  endo- 
carditis, myocarditis,  and  pericarditis.  But  if  one  reflects  on  the  nature  of 
the  symptoms,  such  as  the  condition  of  the  pulse,  its  strength,  rate,  and 
rhythm,  the  size  of  the  heart,  and  the  praecordial  distress — symptoms  which 
are  usually  included  in  the  description  of  endocarditis  and  pericarditis — it 
will  be  realized  that  they  are  not  really  the  manifestations  of  endocarditis 
or  pericarditis,  but  are  the  signs  of  a  myocardial  affection.  One  must 
consider  carefully  the  murmurs  arising  in  the  course  of  a  febrile  attack, 
even  in  rheumatic  fever,  for  the  presence  of  a  murmur  may  not  neces- 
sarily mean  the  invasion  of  the  mitral  valves  by  the  inflammatory 
process,  but  may  be  due  to  the  tonicity  of  the  poisoned  heart  muscle  failing 
and  giving  rise  to  incompetence  of  the  mitral  orifice — due,  therefore, 
not  to  an  endocardial,  but  to  a  myocardial  affection.  Endocarditis  and 
pericarditis,  both  acute  and  chronic,  bulk  so  largely  in  medical  literature 
only  because  an  abnormal  sound  invariably  impresses  the  mind  more  than 
an  abnormal  sign  perceptible  by  the  other  senses,  and  the  easy  recognition 
of  the  valvular  murmur  and  the  friction  sound  has  led  to  the  associated 
symptoms  being  ascribed  to  the  same  lesion. 

§  195.  The  febrile  heart — By  this  term  I  mean  the  changes  induced 
by  the  rise  in  temperature.  The  whole  circulatory  apparatus  is  remark- 
ably sensitive  to  alterations  in  temperature,  whether  arising  from  external 
sources  or  due  to  changes  within  the  body.  The  most  striking  of  these 
is  the  change  in  rate — a  rise  in  temperature  increasing  the  rate,  and 
a  fall  diminishing  it.  In  the  more  simple  febrile  affections  there  is 
a  certain  correspondence  between  the  height  of  the  temperature  and  the 
rate  of  the  heart's  contraction.  Roughly  speaking,  there  is  an  increase  of 
from  eight  to  ten  beats  with  a  rise  of  temperature  of  one  degree  F.  This 
does  not  hold  universally,  but  any  considerable  departure  from  this  rule 
should  always  arouse  watchfulness  and  suggest  the  possibility  of  other 
complications,  such  as  the  involvement  of  the  heart  in  the  infection. 

In  the  simple  febrile  heart  the  radial  artery  enlarges  and  the  pulse  remains 
of  good  strength,  particularly  during  the  diastolic  phase  of  the  cardiac  cycle. 
The  heart  itself  shows  little  change  at  first,  beyond  having  its  rate  abnor- 
mally accelerated  by  exertion.  The  sounds  are  clear  and  distinct,  and  there 
is  no  increase  in  size.  With  long  continuation  of  the  fever  a  certain  amount 
of  dilatation  may  arise.  This  most  readily  occurs  on  the  right  side  of  the 
heart,  particularly  if  the  pulmonary  circulation  is  interfered  with,  as  by 
a  pneumonia  or  a  pleuritic  effusion,  or  by  lying  a  long  time  on  the  back, 
as  during  the  course  of  typhoid  fever.  The  sounds  may  become  feeble,  or 
systolic  murmurs  may  develop  at  the  tricuspid  and  mitral  orifices,  and  the 


216  DISEASES  OF  THE  HEART 

characteristic  pulsation  of  the  right  heart  in  the  epigastrium  become  visible 
(Figs.  29  and  30,  pp.  84,  85).  In  many  of  the  minor  febrile  attacks  the  course 
is  modified  by  the  nature  of  the  toxins  generated.  A  rise  of  a  few  degrees  of 
temperature  may  provoke  an  undue  frequency — 120-140,  and  with  the 
subsidence  of  the  temperature  the  rate  may  speedily  fall  to  normal, 
leaving  no  ill  effects.  A  slight  rise  of  temperature  may  even  be  accompanied 
by  a  fall  in  the  pulse-rate — sometimes,  if  the  patient's  pulse  is  normally 
a  slow  one,  below  fifty  per  minute.  I  have  found  remarkable  variation  in 
rate  with  the  same  temperature  at  different  times,  in  the  same  individual, 
due  probably  to  a  difference  in  the  agent  producing  the  fever.  The  effects 
produced  by  agents  other  than  a  rise  in  temperature  cannot  perhaps  be 
better  illustrated  than  by  those  occurring  during  an  attack  of  ague  ;  here  in 
the  course  of  twenty-four  hours,  with  a  continuously  high  temperature,  we 
have  a  remarkable  series  of  changes  in  the  pulse.  During  the  cold  stage  the 
pulse  becomes  small  and  scarcely  perceptible,  on  account  of  the  contraction 
of  the  peripheral  arteries.  The  blood  driven  from  the  surface  and  from  the 
arterial  system  accumulates  in  the  venous  system  and  in  the  internal  organs. 
Then  the  lips  and  fingers  become  blue,  and  the  congestion  of  internal  organs 
may  reach  such  a  degree  that  capillary  haemorrhages  occur  within  them. 
Within  a  few  hours,  the  temperature  still  being  high,  the  arterioles  relax, 
the  arteries  become  larger,  and  the  pulse  itself  is  of  considerable  force. 

§  196.  Acute  febrile    affections  of  the  heart The  lesion  induced 

by  the  invasion  of  the  heart  by  specific  organisms  is  rarely  limited  to  one 
structure  or  tissue,  so  that  it  would  be  better  to  use  the  term  carditis 
than  to  employ  such  misleading  terms  as  endocarditis  and  pericarditis. 
This  will  be  brought  out  more  clearly  when  an  analysis  is  made  of  the  symp- 
toms present  in  any  given  case,  and  I  shall  endeavour  briefly  to  summarize 
the  symptoms  and  try  to  apportion  them  to  the  particular  tissues  affected. 
I  do  this  here,  because  by  the  appreciation  of  the  nature  of  the  primary  lesion 
we  are  better  able  to  understand"  the  conditions  found  many  years  after, 
when  the  cicatrizing  process  has  wrought  other  changes. 

§  197.  Symptoms  in  myocarditis — The  rate  and  rhythm  are  the 
most  easily  recognized.  Seeing  that  a  rise  of  temperature  alone  induces 
an  increased  frequency,  it  is  impossible  to  apportion  the  relative  influences 
of  this  and  of  the  myocardial  infection.  But  many  cases  of  moderate 
fever  have  a  heart-rate  greatly  accelerated,  and  then  we  can  infer  there  is 
some  other  factor  at  work  than  the  rise  in  temperature.  It  would  be  of 
great  interest  to  know  the  mechanism  by  which  increased  rate  is  brought 
about  by  myocardial  lesions,  whether  through  nerve  stimulation  arising 
reflexly  from  the  inflamed  tissue,  or  from  the  increased  irritabihty  of  the 


ACUTE  FEBRILE  AFFECTIONS  OF  THE  HEART  217 

muscle,  particularly  of  the  tissue  in  which  the  stimulus  for  contraction 
arises.     But  here  such  an  inquiry  would  be  purely  speculative. 

Changes  in  rhythm  come  under  a  different  category,  and  in  irregularity 
we  often  get  a  clue  to  the  changes  that  are  going  on  in  the  muscle.  The 
arrhythmia  due  to  purely  nervous  influences  is  generally  abolished  during 
the  excitation  of  the  heart  by  the  fever — the  chief  exception  being  the 
arrhythmia  due  to  vagus  stimulation  in  affections  of  the  brain  (as  in  tuber- 
cular meningitis). 

The  myocardial  irregularities  have  not  been  as  carefully  worked  out  in 
acute  conditions  as  their  importance  demands,  and  the  slight  advance  I  have 
made  in  the  study  of  the  subject  shows  it  to  be  of  the  utmost  importance 
if  we  would  understand  the  pathology  of  the  living  heart. 

Degression  of  conductivity. — The  most  characteristic  evidence  of  direct 
damage  done  to  the  muscle  of  the  heart  is  the  irregularity  or  pulse  inter- 
mission due  to  the  dropping  out  of  ventricular  systoles,  because  of  the  damage 
done  to  the  a. -v.  bundle  by  the  lesion.  In  carefully  watching  cases  of  rheu- 
matic fever,  I  have  detected  the  appearance  of  a  mitral  murmur,  and  found 
a  lengthening  of  the  interval  between  the  auricular  and  ventricular  systoles, 
followed  later  by  the  presence  of  an  aortic  diastolic  murmur.  The  adminis- 
tration of  digitalis  in  such  cases  has  produced  a  mild  form  of  heart-block 
(Case  27,  Appendix  VI).  This  affection  of  the  a.-v.  bundle,  shown  by  slight 
spontaneous  heart-block,  I  have  detected  in  rheumatic  fever  and  in  influenza 
(Fig.  119),  and  it  has  been  detected  in  otker  acute  affections.  Professor 
Hoist,  of  Christiania,  has  shown  me  tracings  of  mild  heart-block  from 
a  case  of  septic  poisoning,  and  Dr.  Grosh,  of  Toledo,  U.S.A.,  similiar  trac- 
ings from  a  case  of  puerperal  fever,  while  Dr.  Cooper,  of  San  Francisco, 
has  shown  me  tracings  of  complete  heart-block  from  a  case  of  septic 
poisoning  under  the  care  of  Dr.  Jellinek.  In  this  last  case  the  patient  died 
within  fourteen  days  of  the  onset  of  the  heart-block,  and  an  examination 
of  the  heart  by  Dr.  Ophuls  showed  an  anaemic  necrosis  of  the  muscular 
septum  involving  the  a.-v.  bundle,  consequent  on  a  recent  thrombus  of 
the  nutrient  artery. 

In  acute  affections  of  the  heart,  writers  usually  content  themselves  by 
mentioning  irregularity  as  one  of  several  symptoms,  but  the  instances  cited 
show  that  if  graphic  records  were  taken  this  condition  would  be  found 
fairly  frequent. 

Depression  of  contractility. — Towards  the  later  stages  of  fatal  pneu- 
monias, I  have  frequently  detected  a  missed  beat  or  an  irregularity. 
Analysis  of  a  number  of  these  cases  has  shown  that  it  has  probably  been 
due  to  failure  of  the  power  of  contraction.     Thus  a  typical  example  is  seen 


218  DISEASES  OF  THE  HEART 

in  Fig.  137,  where  towards  the  end  of  the  tracing  there  is  shown  a  marked 
pulsus  alternans.  The  missed  beats  in  the  earlier  part  of  the  tracing  I  think 
are  due  to  the  contraction  having  been  so  feeble  that  it  failed  to  propagate 
a  wave  into  the  arteries.     Thus  we  see  in  Fig.  138,  from  another  case  of 


Fig.  137.    Irregular  pulse  in  the  course  of  a  pneumonia,  showing  the  pulsus  alternans  in  the 
latter  half  of  the  tracing.     The  intermissions  may  be  due  also  to  failure  of  contractility. 

pneumonia,  how  the  small  beats  s'  arise  at  the  normal  interval,  but  the 
exhaustion  of  the  heart  is  so  great  that  it  only  sends  out  a  small  quantity 
of  blood,  and  after  the  last  small  beat  it  fails  altogether  to  send  out  a  wave. 
Such  signs  in  pneumonia  I  have  found  always  to  be  of  the  gravest  signi- 


FiG.  138.    Tracmg  of  the  respiratory  curve  and  of  the  irregular  pulse  in  the  course  of  a  fatal 
case  of  pneumonia.    The  small  beats  s^  are  probably  due  to  exhausted  contractility. 

ficance.     John  Hay  has  shown  a  similar  arrhythmia  in  a  patient  suffering 
from  septic  poisoning. 

Extra-systoles. — Extra-systoles  are  of  rare  occurrence  in  severe  infec- 
tious febrile  hearts,  but  Fig.    139  shows  the  occurrence  of  extra-systoles 


Fig.  139.     Extra-systoles  occurring  in  the  course  of  a  fatal  attack  of  rheumatic  fever. 

in  the  course  of  a  fatal  attack  of  rheumatic  fever.  As  there  is  no  com- 
pensatory pause,  the  premature  beat  is  probably  of  auricular  origin  (§  145). 
Nodal  rhythm. — I  have  seen  in  several  instances  the  sudden  inception 
of  this  rhythm  in  pneumonia,  and  always  with  disastrous  results.  In  one 
patient  whom  I  saw  in  consultation  everything  seemed  to  be  progressing 
favourably,  but  while  talking  to  the  doctor  in  attendance  we  were  suddenly 


ACUTE  FEBRILE  AFFECTIONS  OF  THE  HEART  219 

summoned  to  the  bedside  of  the  patient,  and  found  that  the  heart's  action 
had,  in  the  interval  since  our  seeing  him,  taken  on  this  nodal  rhythm,  and 
the  pulse  had  become  rapid  and  irregular.  The  patient  died  a  few  hours 
after.  In  another  case  I  was  called  to  see,  the  doctor  told  me  the  patient 
had  passed  well  through  an  attack  of  pneumonia  terminating  by  crisis. 
The  day  following  the  fall  of  temperature  the  patient  suddenly  became 
weak  and  ill,  and  the  doctor  being  summoned  found  him  collapsed.  I  saw 
him  shortly  after  and  found  the  heart  had  taken  on  the  nodal  rhythm  ;  the 
doctor  assured  me  that  he  had  gone  through  the  pneumonia  with  a  good  and 
regular  pulse.     He  also  died  a  few  hours  after. 

Dilatation  of  the  heart. — Evidences  of  myocardial  affections  can  be 
found  in  the  changes  in  the  size  of  the  heart.  The  symptoms  of  dilata- 
tion have  been  fully  described  in  Chapter  XXIII,  but  it  is  well  to  remember 
that  the  size  of  the  heart  may  very  speedily  become  greatly  increased  in  the 
course  of  a  febrile  affection  of  the  heart,  as  in  rheumatic  fever,  diphtheria, 
&c.  In  such  cases  the  sounds  often  become  very  faint,  and  soft  murmurs 
may  arise  at  the  mitral  and  tricuspid  orifices,  and  simulate  valvular  changes. 

§  198.  Symptoms  in  endocarditis. — The  only  direct  evidence  of  acute 
endocarditis  is  the  presence  of  murmurs  at  one  or  other  orifice  of  the 
heart.  For  practical  purposes  there  are  only  two  murmurs  which  need 
to  be  considered  here,  viz.  a  mitral  systolic  murmur  and  an  aortic  diastolic. 
It  is  not  always  easy  to  tell  whether  the  appearance  of  a  murmur  during 
a  febrile  attack  is  due  to  involvement  of  the  mitral  valve  in  an  endocarditic 
process  or  to  the  relaxation  of  the  muscle  supporting  the  orifice.  A 
diastolic  aortic  murmur  is,  as  a  rule,  diagnostic  of  the  involvement  of 
the  aortic  valve  in  some  destructive  process.  At  first  this  murmur  is  so 
faint  that  one  is  simply  conscious  of  the  fact  that  the  sound  does  not 
end  with  sufficient  abruptness.  Gradually,  however,  this  passes  into 
a  very  soft  short  whiff  at  the  end  of  the  second  sound,  becoming  day  by 
day  more  marked. 

In  the  vast  majority  of  cases  the  murmurs  due  to  endocarditis  are  not 
definitely  recognized  until  some  time  after  the  subsidence  of  the  fever — when 
the  sclerosis  sets  in.  This  is  particularly  the  case  with  presystolic  mitral 
murmurs,  which  are  never  recognized  during  the  acute  condition  that  induces 
the  lesion,  unless  there  is  narrowing  of  the  mitral  orifice  on  account  of  vegeta- 
tions. The  formation  of  vegetations  at  the  mitral  and  aortic  orifices  may 
give  rise  to  murmurs  indistinguishable  from  those  due  to  destruction  of 
the  cusps.  The  presence  of  a  musical  murmur  may  generally  be  assumed, 
particularly  in  acute  cases,  to  be  due  to  a  vegetation.  An  attack  of  hemi- 
plegia during  an  acute  febrile  condition  may  generally  be  ascribed  to  an 


220  DISEASES  OF  THE  HEART 

infarct  from  a  valvular  vegetation,  and  infarcts  in  any  other  organ  may  be 
assumed  to  arise  from  the  same  cause. 

§  199.  Symptoms  in  pericarditis. — Until  the  introduction  of  auscul- 
tation, dry  pericarditis  was  a  disease  only  discovered  on  the  post-mortem 
table.  The  only  evidence  we  have  of  its  presence  is  the  characteristic 
superficial  to-and-fro  murmur  produced  by  the  movements  of  the  heart. 
Its  discovery  is  usually  accidental,  and  made  when  the  heart  is  examined 
as  a  matter  of  routine.  There  is  no  other  distinctive  sign  associated  with  it, 
and,  in  marked  contrast  to  dry  pleurisy,  it  is  essentially  a  painless  complaint. 
When  pains  are  associated  with  its  presence  it  will  invariably  be  found  that 
there  is  evidence  of  a  myocardial  affection.  This  curious  painlessness  of 
pericarditis  compared  with  pleurisy  is  one  that  has  long  puzzled  me,  and 
I  have  only  a  dim  perception  of  how  it  may  arise.  I  merely  call  attention 
to  this  fact  in  passing. 

Pericarditis  may  arise  in  the  course  of  a  number  of  chronic  complaints, 
as  in  diabetes  and  Bright 's  disease,  or  in  the  course  of  an  acute  disease,  as 
pneumonia  or  rheumatic  fever.  Sometimes  one  comes  across  it  quite  acci- 
dentally— the  patient,  not  feehng  quite  well,  consults  his  doctor,  and  in  the 
course  of  an  examination  this  is  detected.  Such  patients  may  go  quietly 
about  their  occupation  for  many  weeks  with  a  well-marked  to-and-fro 
murmur,  and  suffer  no  further  trouble. 

When  effusion  takes  place  into  the  pericardial  sac  there  is  an  increase 
in  the  area  of  the  cardiac  dullness,  which  assumes  a  somewhat  characteristic 
shape.  It  reaches  up  to  or  above  the  second  rib,  and  if  the  area  be  mapped 
out  it  will  have  a  somewhat  pear-shaped  character.  There  is  an  absence 
of  the  heart's  movements  at  the  lower  point  to  the  left,  and  this  should 
always  arouse  the  suspicion  of  effusion  where  there  is  an  increase  in  the  heart's 
dullness.  Ewart  describes  a  small  area  of  dullness  behind  at  the  base  of 
the  left  lung.  This  is  important  to  remember,  for  an  increase  in  the  size 
of  this  area  may  cause  an  extensive  pericardial  effusion  to  simulate  fluid  in 
the  pleural  cavity.  I  have  tapped  a  pericardial  purulent  effusion  in  mistake 
for  an  empyema,  and  my  mistake  arose  from  not  ascertaining  the  position  of 
the  heart's  movements.  Had  the  case  been  one  of  pleural  effusion,  I  should 
have  found  the  heart  beating  to  the  right  of  the  sternum  ;  but  the  whole  left 
chest  was  dull,  so  that  the  idea  of  it  being  pericardial  never  crossed  my  mind. 

The  question  of  pericardial  effusion  embarrassing  the  work  of  the  heart 
has  arisen  on  account  of  the  results  of  experimentally  distending  the  sac 
with  fluid.  I  have  never  found  any  very  serious  embarrassment  of  the 
heart  from  extensive  pericardial  effusion,  the  reason  being  probably  that 
while  the  normal  pericardium  is   a  more  or  less  inelastic  bag,  with   the 


ACUTE  FEBRILE  AFFECTIONS  OF  THE  HEART  221 

inflammatory  invasion  it  becomes  distensile,  and  therefore  able  to  accom- 
modate an  enormous  amount  of  fluid  with  httle  embarrassment  to  the  heart. 

§  200.  The  heart  in  rheumatic  fever — The  real  nature  of  the 
changes  that  take  place  in  acute  affections  of  the  heart  are  being  gradually 
revealed,  and  it  is  now  possible  to  connect  many  of  the  obscure  signs  observed 
during  life  with  the  disease  process  in  the  heart.  Many  workers  have  con- 
tributed to  our  present  knowledge,  but  the  following  description  is  taken 
more  particularly  from  the  observations  of  Cowan  ^^^  and  of  Poynton  and 
Paine  ^22,  as  they  have  sought  with  some  degree  of  success  to  correlate  their 
pathological  findings  with  chnical  and  experimental  data.  These  observa- 
tions have  been  worked  out  more  particularly  in  rheumatic  affections  of  the 
heart  ;  but  similar  changes  have  been  found  in  other  acute  affections,  as 
in  pneumonia,  diphtheria,  influenza,  septic  poisoning. 

According  to  Po3niton  and  Paine,  the  heart  trouble  starts  with  the  inva- 
sion of  the  heart  by  the  specific  organism  of  rheumatic  fever — the  Diplococcus 
rheumaticus.  (Many  later  investigators  have  failed  to  isolate  this  organism.) 
They  reckon  to  have  isolated  this  organism  from  vegetations  found  on 
the  valves  of  the  heart  and  pericardium  in  acute  rheumatism,  have  cultivated 
it,  and  produced  changes  in  animals  identical  with  rheumatic  endocarditis, 
myocarditis,  and  pericarditis.  The  invasion  of  the  endocardium  usually 
affects  first  the  base  of  the  valves,  and  produces  sweUing  and  infiltration  of 
the  margins.  The  swollen  edges  may  break  down  and  ulcerate,  or  vege- 
tations may  form.  The  course  of  the  disease  varies  greatly,  from  the  simple 
endocarditis  which  recovers,  to  extensive  ulceration  of  the  valves,  associated 
with  the  severe  symptoms  characteristic  of  malignant  endocarditis. 

The  myocardium  rarely  escapes,  and  the  changes  in  it  are  of  great 
importance,  both  for  the  acute  condition  and  for  the  subsequent  integrity 
of  the  heart  muscle.  Fatty  degeneration  and  breaking  down  of  the 
muscle-fibres  are  fairly  common,  while  the  specific  organism  has  been 
found  accompanied  by  cellular  infiltration.  There  may  be  congestion  of 
the  blood-vessels,  exudation  of  the  leucocytes,  and  swelling  of  the  connective 
tissues.     Aschoff  ^^^  describes  the  occurrence  of  numerous  cellular  foci. 

During  the  acute  attack  extreme  dilatation  may  occur,  due  probably  to 
a  toxaemic  poisoning  of  the  heart  muscle,  as  no  microscopic  change  may 
be  present.  This  poisoning  is  probably  also  the  cause  of  the  extreme  weak- 
ness and  irritability  of  the  heart,  which  persists  for  some  time  after  the  subsi- 
dence of  the  fever.  The  pericardium  is  also  liable  to  invasion,  and  here  the 
changes  may  vary  from  a  shght  transient  pericarditis  to  an  extreme  inflam- 
mation, which  does  not  entirely  subside,  but  lingers  on,  forming  adhesions, 
to  the  tissue  outside  the  pericardium  and  penetrating  to  the  heart  itself. 


222  DISEASES  OF  THE  HEART 

A  process  of  slow  cicatrization  often  follows,  producing  changes  in  the 
valves,  heart  muscle,  and  pericardium  that  seriously  embarrass  the  heart 
in  its  work  in  after  years. 

Symptoms. — x4ttacks  of  rheumatic  fever  may  complete  their  course 
with  no  affection  of  the  heart.  In  some  instances  the  heart  may  be  affected 
and  give  rise  to  no  positive  sign,  and  it  may  be  only  after  months  or  years 
that  a  murmur  or  irregular  action  indicates  that  there  must  have  been 
some  affection  of  the  heart  which  the  symptoms  of  the  subsequent  sclerosing 
process  has  revealed. 

Generally,  however,  we  can  recognize  certain  changes  in  the  heart's 
condition,  chiefly  in  an  increase  in  the  size  and  the  presence  of  a  murmur. 
These  cardiac  changes  may  go  on  with  very  little  increase  of  temperature 
and  little  or  no  evidence  of  joint  trouble.  Sometimes  in  these  milder  cases 
I  have  detected  evidence  of  involvement  of  the  a.-v.  bundle  by  signs  of 
interference  with  its  power  of  conveying  the  stimulus  from  auricle  to  ventricle. 

With  more  serious  involvement  the  dilatation  of  the  heart  may  be 
extreme,  and  Lees  and  Poynton  1^°  particularly  have  called  attention  to  the 
enlargement,  and  the  ease  with  which  it  may  be  mistaken  for  pericardial 
effusion.  At  first,  the  full  extent  of  the  enlargement  may  not  be  realized, 
because  it  is  partly  masked  by  the  lung.  When  the  lung  is  pushed  aside, 
the  greatly  enlarged  heart  can  then  be  readily  recognized.  The  rate  of  the 
heart  is  usually  greatly  increased  beyond  what  might  be  expected  from 
a  mere  rise  in  temperature.  The  pulse  becomes  soft  and  compressible,  and 
sometimes  shows  irregularities  whose  nature  in  all  cases  I  have  not  been 
able  to  make  out.  With  subsidence  of  the  fever,  the  patient  enters  on 
a  long  and  slow  convalescence.  Other  cases  do  not  terminate  so  favour- 
ably, especially  if  the  heart  has  been  damaged  by  a  previous  attack.  Com- 
plications, as  pneumonia,  are  apt  to  arise.  In  severe  cases  there  may 
be  a  considerable  amount  of  praecordial  distress.  The  breathing  becomes 
shallow  and  rapid.  The  patient  feels  easiest  with  his  shoulders  well  raised. 
The  face  becomes  dusky,  the  lips  dark  red,  sleep  is  broken  and  fitful,  and 
the  patient  is  continuously  altering  his  position.  The  mind  wanders  and 
mental  delusions  arise. 

From  such  a  state  as  this  the  young  during  their  first  attack  may  recover, 
but  in  the  middle-aged  the  condition  is  very  serious.  Attacks  of  syncope 
may  appear,  and  the  patient  may  die  in  one.  Frequently  they  gradually 
sink  in  spite  of  all  treatment  and  die. 

In  the  recurring  attacks  of  rheumatic  fever  this  question  of  previous 
damage  to  the  heart  is  a  very  important  one.  Patients  with  damaged 
aortic  and  mitral  valves  may  pass  scatheless  through  serious  attacks  of 


ACUTE  FEBRILE  AFFECTIONS  OF  THE  HEART  223 

rheumatic  fever,  presumably  where  the  heart  is  not  involved  in  these  later 
attacks.  When,  however,  the  process  lays  hold  on  the  heart,  the  patient's 
life  is  in  great  danger,  and  after  a  period  of  extreme  suffering  the  struggle 
frequently  ends  in  death. 

While  the  foregoing  description  gives  briefly  the  main  points  of  the  heart 
affection  in  rheumatic  fever,  it  also  holds  good  for  the  condition  in  other 
infectious  diseases,  apart  from  the  recurrent  attacks.  As,  however,  the 
presence  of  other  lesions  has  a  modifying  effect  upon  the  course  of  the 
disease,  it  is  necessary  to  refer  to  them.  Unfortunately,  the  reference  can 
only  be  brief  and  in  the  main  unsatisfactory,  the  analysis  of  the  symptoms 
in  these  cases  having  been  very  imperfectly  carried  out. 

§  201.  The  heart  in  pneumonia — The  invading  organism  may  assail 
the  heart  as  well  as  the  lungs,  and  the  course  of  the  illness  be  rapid  and 
severe.     It  is  difficult  to  distinguish  between  the  changes  due  to  invasion 


Fig.  140.  Febrile  pulse  of  low  arterial  pressure,  T.  103°,  P.  116,  R.  36.  This  was  taken 
eight  hours  after  the  rigor  at  the  beginning  of  a  pneumonia.  This  and  the  four  following 
tracings  show  a  type  of  asthenic  pulse. 

of  the  heart  from  those  due  to  the  general  infection.  In  severe  cases  the 
evidence  of  the  heart  affection  is  very  prominent.  Within  a  few  hours 
of  the  initial  rigor,  and  before  there  is  any  pulmonary  sign,  the  evidence  of 
the  heart  affection  is  all  too  apparent.  The  patient  may  be  young  and, 
prior  to  the  attack,  a  perfect  specimen  of  youthful  health  and  vigour.  A  few 
hours  after  the  rigor,  the  temperature  may  be  over  102°  F.  The  condition 
of  the  pulse  is  the  best  guide  to  the  state  of  the  heart  at  this  stage,  and  shows 
ominous  signs  of  what  is  to  follow.  It  is  greatly  increased  in  rate,  115-130 
per  minute.  It  is  soft  and  compressible,  and  offers  no  resistance  between 
the  beats.  The  peculiar  manner  in  which  it  impinges  against  the  finger — 
sharp  and  short,  then  quickly  subsiding,  indicating  an  absence  of  sustained 
pressure — is  always  to  me  a  serious  sign.  It  is  usually  associated  with  greatly 
relaxed  arteries,  and  a  sphygmogram  shows  little  or  no  sign  of  a  dicrotic 
wave  (Figs.  140-4),  indicating  great  lowering  of  the  pressure  during  the 
diastole  of  the  heart.  The  heart  itself  shows  little  definite  sign.  The  sounds 
are  short  and  sharp  at  first,  becoming  later  somewhat  muffled,  A  certain 
amount  of  dilatation  occurs,  detected  more  particularly  to  the  right  of  the 
sternum.  Usually  in  these  cases  the  end  comes  with  tragic  suddenness  ; 
the  rate  of  the  pulse  increases,  irregularities  appear,  and  the  patient  succumbs 


224 


DISEASES  OF  THE  HEART 


within  three  or  four  days  of  the  initial  rigor.  Figs.  140-4  show  the  charac- 
teristic features  of  the  pulse  in  acute  fatal  pneumonia  in  a  young  previously 
strong  and  healthy  adult. 

There  are  two  conditions  I  have  come  to  look  upon  as  signs  of  grave 
comphcations  in  pneumonia — the  occurrence  of  an  occasional  irregularity 
before  the  crisis,  and  a  pulse-rate  over  140  per  minute.     Neither  of  these  is 


Fig.  141.     T.  101-5°,  P.  96,  R.  28— second  day. 


Fig.  142.     Asthenic  type  of  pulse  with  well-marked  systoUc  wave  s,  and  only  a  faint  indi- 
cation of  the  dicrotic  wave  d — third  day. 


Fig.    143.     T.    103°,    P.    124,    R.    48— fourth   day. 


Fig.  144.     T.  102°,  P.  148,  R.  52.     The  irregularity  and  rapidity  of  the  pulse  heralded  the 

fatal  end  on  the  fifth  day. 

necessarily  a  fatal  symptom.  I  had  pointed  this  out  in  my  book  on  the  pulse, 
and  John  Hay*"^^  analysing  200  cases  of  pneumonia,  found  a  small  number 
recover  who  had  shown  an  irregularity  preceding  the  crisis.  I  therefore 
went  into  the  matter  more  carefully,  and  found  that  the  occasional  irregu- 
larity might  be  due  to  more  conditions  than  one,  and  in  all  my  fatal  cases 
the  irregularity  was  due  to  exhaustion  of  the  contractiUty,  as  shown  in  Figs. 
137  and  138  ;   but  this  subject  needs  further  elucidation. 

§  202.  The    heart    in   diphtheria — The    comphcations    here    are    so 


ACUTE  FEBRILE  AFFECTIONS  OF  THE  HEART 


225 


varied  that  danger  may  arise  in  several  quarters.  The  heart  muscle  itself 
may  be  the  seat  of  profound  changes,  the  symptoms  somewhat  resembUng 
those  in  rheumatic  fever.  But  in  diphtheria  more  than  in  any  other  acute 
disease  there  is  a  tendency  to  fatal  syncope,  and  I  do  not  understand  how 
this  is  brought  about. 

§  203.  Septic  infections. — There  are  a  great  many  septic  infections 
that  injure  the  heart  either  from  toxaemia  or  by  a  specific  organism  invading 
the  heart.  In  the  latter  case  the  endocardium  is  frequently  attacked,  and 
the  disease  is  then  described  as  septic  endocarditis.  In  these  cases  there 
is  also  invasion  of  the  myocardium,  and  it  is  the  profound  depression  of  the 
heart  muscle  which  is  often  the  grave  element. 

In  an  account  of  150  cases  of  infective  endocarditis,  Horder*''^  states  that 
in  90  per  cent,  of  cases  a  culture  of  a  pathogenic  organism  can  be  obtained. 
The  following  table  gives  the  analysis  of  forty  positive  results  of  blood 
culture  during  hfe  : — 


Number  of  Cases. 
26 
5 
5 
2 
1 
I 


Micro-organism  isolated. 

Streptococcus 
Bacillus  influenzae 
Pneumococcus 
Gonococcus 
Staphylococcus  albus 
Unclassified. 


The  illness  in  these  cases  usually  begins  insidiously,  and  at  first  may  be 
mistaken  for  some  trivial  febrile  complaint,  or  for  influenza.  Soon,  however, 
the  extreme  prostration  of  the  patient,  the  recurrence  of  rigors,  and  the 
patient's  own  sensation  of  illness,  show  that  the  condition  is  of  a  more 
serious  nature.  Usually  also  there  is  excessive  perspiration.  If  the  heart  be 
watched  it  will  be  found  to  dilate  and  a  systolic  murmur  appear.  The  true 
nature  of  the  condition  may  not  be  revealed  until  the  detachment  of  a  vege- 
tation produces  hemiplegia,  or  an  infarct  in  the  spleen  or  kidney  or  elsewhere, 
and  death  may  speedily  supervene  (malignant  endocarditis). 

Other  cases  may  Hnger  on  with  indefinite  febrile  attacks,  the  patient 
sick,  pale,  and  ill,  and  the  real  nature  of  the  illness  be  a  mystery.  In  some 
of  these  cases  very  little  change  takes  place  in  the  heart.  I  have  seen  a  case 
after  confinement  have  slight  fever  for  nine  weeks  with  no  change  in  the 
size  of  the  heart,  the  rate  generally  about  eighty  per  minute,  a  rough  systolic 
mitral  murmur  the  only  abnormal  sign,  until  an  attack  of  hemiplegia  led 
to  the  recognition  that  the  rough  mitral  murmur  was  due  to  vegetations  on 
the  valves.     Osier  ^^^  has  recently  published  an  account  of  ten  cases  of  chronic 


MACKEXZIE 


226  DISEASES  OF  THE  HEART 

infectious  endocarditis.  In  addition  to  the  irregular  fever  he  gives  the 
following  as  the  most  suggestive  features  which  help  to  identify  the  nature 
of  the  disease.  (1)  A  knowledge  of  the  existence  of  an  old  valve  trouble; 
(2)  the  occurrence  of  embolic  features,  sudden  swelhng  of  the  spleen,  sudden 
attack  of  haematuria,  embohsm  of  the  retinal  arteries,  hemiplegia,  or  the 
blocking  of  a  vessel  in  one  of  the  limbs ;  (3)  the  onset  of  special  skin  symptoms, 
purpura,  and  more  particularly  the  painful  erythematous  nodules,  in  aU 
probabihty  due  to  minute  emboli  ;  (4)  the  progressive  cardiac  changes, 
the  gradual  increase  in  the  dilatation  of  the  heart,  the  marked  change  in  the 
character  of  the  mitral  murmur,  the  onset  of  a  loud  rasping  tricuspid  murmur, 
or  the  development  under  observation  of  an  aortic  diastolic  bruit. 

In  pyaemia  and  puerperal  septicaemia  we  get  conditions  of  profound 
gravity  caused  by  certain  organisms.  The  pulse  in  these  cases  gives  the 
most  trustworthy  information.  It  is  small,  soft,  and  easily  compressed, 
not  necessarily  very  rapid,  and  the  temperature  need  not  be  high  (101-2°). 
The  heart  shows  little  change  except  that  the  sounds  are  feeble,  the  patient 
is  lethargic,  the  face  is  slightly  sallow  or  pale  and  sunken.  The  aspect  of 
the  patient,  taken  with  the  rate  of  the  pulse,  affords  assistance  in  recognizing 
the  condition.  I  dwell  upon  this  because,  happily,  some  of  the  younger 
members  of  the  profession  have  Uttle  experience  of  dangerous  forms  of 
puerperal  fever,  but,  having  heard  of  the  terrors  surrounding  them,  are  not 
infrequently  unnecessarily  frightened  at  the  occurrence  of  a  post-partum 
rise  of  temperature  of  trivial  significance,  while  others  do  not  recognize  the 
significance  of  the  heart  symptoms  when  danger  actually  arises. 

§  204.  Treatment. — When  the  real  nature  of  the  trouble  is  appreciated 
in  acute  affections  of  the  h^rt,  it  will  be  realized  how  powerless  we  are 
directly  to  modify  the  diseased  process.  In  vaccine  or  serum  therapy  there  is 
a  promise  of  a  specific  remedy  in  each  case  to  meet  the  special  organism 
causing  the  mischief.  But  so  far  our  efforts  have  been  attended  with  httle 
success.  Horder  *°^  states  that  of  thirty-nine  cases  treated  in  this  way  only 
one  recovered,  and  unfortunately  in  this  case  no  micro-organism  was  demon- 
strated in  the  blood.  He  says,  '  I  have  given  the  treatment  most  thorough 
trial  in  several  cases,  and  occasionally  seen  temporary  improvement  result, 
but  never  any  permanent  good.  Conder^^^  has  recently  described  a  case 
where  the  recovery  seemed  directly  due  to  the  vaccine  injection. 

In  rheumatic  fever  the  sahcylates  seem  to  have  an  undoubted  action  on 
the  course  of  the  disease,  and  it  may  be  that  the  drug  can  modify  the  heart 
affection.  Their  employment  is  so  frequently  of  use  that  it  should  always 
be  tried,  even  pushing  it  at  times  as  Lees  advocates.  I  have  not  given  the 
large  doses  of  the  salicylates  recommended  by  Lees  in  a  sufficient  number 


ACUTE  FEBRILE  AFFECTIONS  OF  THE  HEART  227 

of  cases  to  be  able  to  dogmatize,  but  as  the  few  in  which  I  have  followed 
his  directions  seemed  to  get  benefit,  I  have  included  in  Chapter  XXXIII 
a  short  account  by  Dr.  Lees  of  the  method  he  pursues. 

Apart  from  the  probably  specific  action  of  salicylate  in  rheumatic  cases, 
the  employment  of  cardiac  or  other  drugs  is  of  httle  avail.*  The  heart  is 
already  in  possession  of  a  poison  far  more  powerful  than  the  drugs  at  our 
command,  and  these  in  medicinal  doses  are  without  effect.  But  on  this 
account  it  must  not  be  supposed  that  all  treatment  is  useless  ;  rather  should 
it  direct  our  attention  to  the  consideration  of  other  means  of  treatment.  The 
man  who  puts  his  faith  in  drugs  exclusively  neglects  too  often  the  most 
useful  methods.  Recognizing  that  the  heart  muscle  is  greatly  embarrassed 
in  its  work,  the  endeavour  should  be  n^^ade  to  give  it  as  little  work  to  do  as 
possible,  and  to  save  it  from  all  sources  of  irritation  ;  in  fact,  to  place  it  in 
a  condition  of  rest,  as  far  as  rest  is  possible  for  such  an  active  organ  as  the 
heart.  To  this  end  the  general  condition  of  the  patient  should  be  carefully 
studied,  the  position  he  assumes  should  be  one  that  gives  the  heart  least  work 
to  do,  the  food  should  be  so  administered  that  while  nourishing  him  it  does 
not  lead  to  abdominal  distension,  his  bowels  should  be  so  regulated  as  to 
act  freely  without  straining.  As  fidgeting  and  restlessness  keep  the  heart 
irritable  and  variable  in  its  action,  everything  should  be  done  for  his  bodily 
comfort — sponging,  and  arranging  his  piUows  and  the  bedclothes,  and  the 
many  Httle  things  that  a  deft  and  intelligent  nurse  can  suggest.  Above 
all,  sleeplessness,  which  is  so  often  present,  or  the  sleep  that  is  broken  and 
disturbed,  should  have  most  careful  consideration,  and  suitable  hypnotics 
be  given  as  described  in  Chapter  XXXIII. 

AVhen  there  is  reason  to  suspect  that  the  heart  muscle  has  been  affected 
by  the  illness,  great  care  should  be  taken  during  the  convalescence  to  give 
the  heart  muscle  time  to  recover.  Any  cause,  effort  or  excitement,  that 
accelerates  the  heart's  action,  should  be  avoided,  and  exertion  only  per- 
mitted when  the  dilatation  has  subsided,  and  effort  ceases  to  call  forth 
any  disagreeable  sensation.  It  may  be  weeks  or  months  after  the  fever 
before  the  heart  muscle  recovers. 

*  Hordei'  says :  '  "  Blood  antiseptics  "  seem  doomed  to  failure  in  dealing  with  pyogenic  blood 
infections,  because  it  is  not  possible  to  get  the  drugs  into  the  blood  in  a  nascent  or  active 
condition.  Combination  with  the  proteids  of  the  blood-cells  or  the  plasma  takes  place  before 
the  drug  comes  into  contact  with  the  micro-organism.  Quinine,  mercury,  arsenic,  carbolic 
acid,  formalin,  and  many  other  reputed  remedies,  all  fail,  whether  administered  by  the  mouth, 
subcutaneously ,  or  intravenously.  The  sulpho-carbolates  which  have  had  a  special  vogue  are 
equally  disappointing ;  I  have  used  them  in  very  large  doses  in  several  cases  without  any 
results.  Silver  salts  in  combination  with  nuclein  have  been  highly  spoken  of  in  the  treatment 
of  septicaemia,  but  here  again  I  have  never  seen  any  good  results  in  infective  endocarditis. 
The  same  remarks  apply  to  yeast  and  its  active  principle.' 

Q  2 


CHAPTER   XXV 

Valvular  Defects 

§  205.     The  manner  of  heart  failure  with  vali^ular  defects. 

Mitral  stenosis. 

206.  Conditions  inducing  heart  failure  in  mitral  stenosis. 

207.  Murmurs  present  in  mitral  stenosis  (presystolic,  diastolic,  disappearance  of  the  pre- 

systolic murmur,  presystolic  murmur  of  ventricular  origin,  systolic  murmur  due 
to  mitral  stenosis). 

208.  Progress  and  s3Tnptoms  in  mitral  stenosis. 

209.  Occasional   symptoms :     paroxysmal   tachycardia,    haemoptysis,    cerebral  embolism, 

angina  pectoris. 

Mitral  regurgitation. 

210.  Murmurs  due  to  mitral  regurgitation. 

211.  Conditions  inducing  heart  failure  in  mitral  regurgitation. 

§  205.  The  manner  of  heart  failure  with  valvular  defects It  is 

manifest  that  valvular  defects  can  embarrass  the  work  of  the  heart  in  two 
ways  :  first,  by  narrowing  the  orifice  and  thereby  impeding  the  outflow  ; 
second,  by  imperfect  closure  so  that  leakage  occurs. 

The  defects  are  recognized  clinically  mainly  by  the  presence  of  murmurs, 
but  it  must  not  be  assumed  that  absence  of  murmurs  implies  an  intact 
valvular  apparatus,  for  great  widening  of  an  orifice  and  large  regurgitation 
may  take  place  when  no  murmur  can  be  detected.  As  valvular  lesions  are 
produced  by  a  variety  of  conditions,  it  might  have  been  more  logical  to  discuss 
them  under  the  heading  of  these  conditions.  As,  however,  they  are  pre- 
sented to  us  at  a  stage  when  all  immediate  symptoms  of  their  causal  con- 
dition are  in  abeyance,  it  is  more  convenient  to  describe  them  at  the  time 
that  the  heart-changes  evoke  symptoms  of  exhaustion.  Years  may  elapse 
after  the  mischief  has  been  done  to  the  valves  before  symptoms  arise  that 
call  attention  to  the  heart  trouble.  In  the  acute  condition  producing  the 
valvular  lesion,  the  matter  is  presented  in  an  entirely  different  aspect,  for 
the  febrile  state  and  the  symptoms  associated  with  the  cause  of  the  fever 
predominate.  In  chronic  valvular  affection  the  symptoms  only  arise  where 
exhaustion  of  the  heart  muscle  sets  in.  The  symptoms  due  to  exhaustion 
appear  at  varying  periods  after  the  damage  has  been  done  to  the  valves, 
and  the  time  of  the  appearance  of  these  symptoms  depends  on  the  degree  of 
embarrassment  offered  to  the  heart's  work  by  the  damaged  valve,  on  the 


VALVULAR  DEFECTS  229 

condition  of  the  muscle-wall,  and  on  such  accessory  factors  as  tend  to 
exhaustion,  as  over-exertion,  excessive  food,  drink,  and  so  forth. 

In  organic  lesions  of  the  valves  it  must  always  be  borne  in  mind  that  the 
sclerotic  process  causing  the  lesions  may  be  progressive,  and  that  there 
may  also  be  present  advancing  changes  in  the  heart  muscle. 

Generally  speaking,  the  symptoms  of  heart  failure  show  little  that  is 
distinctive  of  the  particular  valves  affected.  In  the  aortic  cases  the  reflex 
sensory  phenomena  are  more  prominent,  and  the  ashen  colour  of  the  face 
is  sometimes  characteristic.  Where  there  is  a  mitral  lesion,  the  pulmonary 
symptoms  are  usually  more  prominent,  and  the  face  may  be  ruddy  with 
a  dark  tinge.  Apart  from  such  differences  there  is  a  great  similarity  in  the 
symptoms  of  heart  failure  produced  by  all  kinds  of  lesions. 

Mitral  Stenosis 

§  206.  Conditions   inducing   heart   failure   in   mitral   stenosis. — 

This  is  perhaps  the  most  common  of  valvular  defects  with  which  heart 
failure  is  associated.  It  arises  generally  in  consequence  of  rheumatic  endo- 
carditis, though  it  may  be  found  in  people  with  no  rheumatic  history,  and 
a  previous  history  of  erysipelas,  or  some  other  febrile  complaint,  may  give 
a  possible  clue  to  its  origin. 

The  condition  is  never  recognized  during  the  acute  process  which  induces 
it,  for  the  reason  that  its  presence  can  only  be  detected  when  the  cicatrizing 
process  following  the  inflammation  narrows  the  orifice,  and  on  account  of 
its  origin  in  scar-formation  it  is  often  a  progressive  lesion.  Once  the  stenosis 
is  present  it  may  remain  moderate  in  amount,  and  offer  so  little  embarrass- 
ment to  the  heart  that  patients  may  reach  extreme  old  age  with  no  heart 
failure.  As  a  rule,  however,  the  cicatrizing  process  goes  on  with  varying 
rapidity  until  in  some  cases  the  mitral  orifice  is  reduced  to  a  mere  slit,  and 
the  valves  resemble  a  thickened  calcareous  diaphragm.  It  is  important  to 
bear  in  mind  the  progressive  nature  of  the  lesion,  for  it  accounts  for  the 
varying  changes  in  the  symptoms.  It  should  also  be  borne  in  mind  that  the 
cicatrizing  process  may  be  going  on  in  the  muscle,  causing  contraction  of 
the  chordae  tendineae,  impairing  at  other  places  the  functional  activity  of 
the  heart  muscle,  and  affecting  the  a. -v.  bundle,  depressing  the  conductivity 
or  producing  the  nodal  rhythm,  thereby  profoundly  modifying  the  nature 
of  the  rhythm  of  the  heart. 

From  this  it  can  readily  be  understood  that  the  manner  in  which  heart 
failure  is  brought  about  in  many  cases  is  somewhat  complicated.  In  some, 
embarrassment  may  not  ensue  until  the  narrowing  of  the  orifice  has  become 
extreme.     In  others  there  may  be  a  fatal  issue  while  the  harrowing  is  yet 


230  DISEASES  OF  THE  HEART 

moderate.  In  the  latter  cases  the  muscle-wall  will  inevitably  be  found  to  have 
been  damaged.  In  a  third  class  of  case  the  cicatrizing  process  has  extended  to 
the  a.-v.  bundle,  and  encroaching  on  it  has  induced  the  nodal  rhythm,  charac- 
terized sometimes  by  greatly  increased  frequency  of  the  heart's  action, 
and  usually  by  a  continuous  irregularity  (see  Chapter  XX).  This  irregular 
action  further  embarrasses  the  heart  muscle  in  carrying  on  its  work,  as 
alread}^  described.  The  mechanical  embarrassment  may  not  only  lead  to 
increasing  back-pressure  involving  in  succession  the  left  auricle,  pulmonary 
circulation,  and  right  heart,  but  the  smaU  quantity  of  blood  passing  into 
the  left  ventricle  leads  to  the  tissues  generally  being  poorly  nourished.  The 
left  ventricle,  suffering  hkewise  from  an  impoverished  supply  of  blood,  may 
offer  independent  symptoms  of  exhaustion,  as  for  instance  by  dilating 
(exhaustion  of  tonicity),  and  possibly  by  reflex  phenomena,  as  in  the  rare 
instance  of  an  attack  of  angina  pectoris  in  mitral  stenosis. 

§  207.  The  murmurs  present  in  mitral  stenosis.  The  presystolic 
murmur. — The  presystolic  murmur — the  auricular  systohc  murmur  of 
Gairdner^^^ — is  due  to  the  contraction  of  the  left  auricle  forcing  blood 
through  the  narrowed  mitral  orifice.  With  the  varying  changes  in  advancing 
cicatrization  the  murmurs  of  mitral  stenosis  alter,  and  present  pecuharities 
that  have  hitherto  not  been  sufficiently  appreciated.  In  the  very  early 
stages, — some  years  before  the  appearance  of  a  murmur, — I  have  detected 
a  slight  presystolic  thrill.  The  first  murmur  to  appear  precedes  or  runs  up 
to  and  seems  to  terminate  in  the  first  sound,  and  is  audible  over  a  small  area 
around  the  apex.  Tliis  murmur  may  vary  in  duration,  being  usually  short 
and  abrupt,  but  it  sometimes  begins  earlier  and  is  somewhat  prolonged.  It 
is  of  a  crescendo  character,  rising  in  pitch  till  it  ends  in  the  first  sound. 
Now  although  this  is  the  usual  position  in  the  cardiac  cycle  of  the  pre- 
systolic murmur,  I  have  found  a  few  cases  in  which  it  did  not  terminate 
abruptly  in  the  first  sound,  but  was  separated  from  it  by  a  very  brief 
interval.  In  some  of  my  cases  I  asked  a  number  of  my  colleagues  to  mark 
out  on  a  tracing  of  the  radial  pulse  the  exact  position  of  the  murmur  in 
the  cardiac  cycle,  and  every  one  without  hesitation  indicated  the  position 
as  represented  in  Fig.  112,  where  the  loudest  part  of  the  murmur  is  separated 
by  a  minute  interval  from  the  first  sound.  When  a  jugular  or  an  apex 
tracing  was  taken  it  was  seen  that  the  position  was  identical  with  that  of 
the  auricular  systole.  In  other  words,  there  was  a  delay  in  the  transmission 
of  the  stimulus  for  contraction  between  auricle  and  ventricle.  This  delay 
can  sometimes  be  increased  by  digitalis,  and  the  position  of  this  murmur 
in  its  relation  to  the  first  sound  moves  in  the  same  way. 

I  mention  this  not  only  to  enforce  the  evidence  of  changes  in  the  a.-v. 


VALVULAR  DEFECTS  231 

bundle  in  mitral  stenosis,  but  because  some  clinicians  deny  that  the  auricular 
systole  causes  the  presystohc  murmur  in  mitral  stenosis.  I  have  long  been 
puzzled  to  account  for  their  denial  of  what  seems  so  obvious,  but  I  have 
found  what  seems  to  be  the  explanation,  and  will  deal  with  it  after  describing 
the  murmurs  with  the  nodal  rhythm. 

The  diastolic  murmur. — With  advancing  stenosis  of  the  orifice  another 
murmur  makes  its  appearance,  namely,  one  occurring  immediately  after 
the  second  sound,  heard  only  in  the  immediate  neighbourhood  of  the  apex 
beat.  At  first  it  is  very  faint,  and  not  very  constant,  but  it  usually  increases 
in  duration  until  the  whole  diastolic  period  may  be  filled  up  by  it.  This 
diastolic  mitral  murmur  diminishes  in  intensity  from  the  beginning — 
differing  thus  in  its  diminuendo  character  from  that  of  the  presystolic. 
Frequently  we  can  detect  a  continuous  murmur  during  the  diastole  of  the 
heart,  beginning  loudly,  falling  away,  then  increasing  in  intensity.  The 
fkst  or  diminuendo  portion  of  such  a  murmur  is  the  diastoHc  mitral  murmur, 
while  the  terminal  crescendo  portion  is  the  presystohc.  The  cause  of  the 
diminuendo  diastolic  mitral  murmur  is  the  flow  of  the  blood  that  has  been 
accumulated  in  the  auricle  during  the  ventricular  systole  through  the 
narrowed  mitral  orifice  ;  this  begins  as  soon  as  the  mitral  valves  open,  that 
is,  when  the  pressure  in  the  ventricle  falls  below  that  in  the  auricle. 

The  disappearance  of  the  presystolic  murmur. — The  next  change  in 
the  character  of  these  murmurs  is  the  sudden  disappearance  of  the  pre- 
systolic crescendo  murmur,  while  the  diastolic  murmur  persists.  Usually 
this  change  occurs  with  the  onset  of  grave  symptoms  of  heart  failure,  the 
heart's  action  becoming  rapid  and  irregular.  At  other  times  the  change 
takes  place  with  no  serious  symptom,  but  the  heart  invariably  becomes 
irregular.  I  have  explained  this  fully  in  Chapter  XX  and  in  the  Appendix 
(II),  as  being  due  to  the  fact  that  the  rhythm  of  the  heart  starts  no  longer  at 
the  normal  place  but  lower  down,  perhaps  at  the  a. -v.  node,  and  that  in 
consequence  the  auricular  contraction  no  longer  precedes  the  ventricular, 
but  the  auricles  and  ventricles  contract  together.  Clinicians  hitherto  have 
not  recognized  the  fact  that  in  mitral  stenosis  the  presystolic  murmur 
disappears  with  the  onset  of  the  continuous  irregularity  of  the  heart. 

When  the  heart's  action  is  slow  there  is  no  difficulty  in  recognizing  the 
diastohc  murmur,  and  the  absence  of  the  presystolic.  The  diastolic  murmur 
is  sometimes  of  great  length,  starting  immediately  after  the  first  sound,  and 
slowly  dying  away,  as  in  Fig.  57.  When  the  heart's  action  is  rapid,  this 
diastohc  murmur  may  fill  up  the  whole  diastohc  pause,  and  it  might  hastily 
be  assumed  that  the  murmur  was  presystolic.  But  if  it  be  carefully  auscul- 
tated, it  will  be  found  that  it  is  not  crescendo  in  character  ;   when  a  longer 


232  DISEASES  OF  THE  HEART 

pause  occurs  it  will  be  found  that  the  murmur  stops  short  before  the  first 
sound,  so  that  there  is  a  silence  between  the  end  of  the  murmur  and  the 
first  sound  (see  shading  in  Fig.  57),  In  these  cases  the  jugular  and  liver 
pulses  are  invariably  of  the  ventricular  form. 

The  presystolic  murmur  of  ventricular  origin. — In  the  careful  examination 
of  a  large  number  of  these  cases  of  nodal  rhythm  we  find  that  the  first  sound 
has  not  the  sonorous  rumble  of  the  normal  first  sound,  but  is  represented 
by  a  sharp,  short  snap  of  very  brief  duration.  Preceding  this  snap,  in  a 
very  few  cases  I  have  heard  a  brief  crescendo  murmur,  but  a  venous  tracing 
showed  that  there  was  no  auricular  systole  at  the  normal  time.  From  this 
I  suggest  that  the  disputants  in  the  matter  have  hitherto  been  confusing 
two  separate  conditions.  As  I  have  already  pointed  out,  the  evidences  of 
auricular  systole  producing  a  presystolic  murmur  are  indisputable.  While 
the  auricular  systole  is  one  cause,  it  is  obvious  there  must  be  another 
cause  in  these  cases  of  nodal  rhythm,  and  I  therefore  accept  the  view  that 
a  slight  regurgitation  through  the  mitral  orifice  at  the  beginning  of  ven- 
tricular systole  may  produce  the  brief  presystohc  murmur.  (As  a  matter 
of  fact  such  a  murmur  does  not  precede  the  ventricular  systole,  but  only 
precedes  that  portion  of  the  first  sound  represented  by  the  terminal  snap). 

Systolic  murmur  due  to  mitral  stenosis. — There  is  another  form  of 
murmur  associated  with  mitral  stenosis,  systolic  in  time,  and  heard  best 
at  the  apex.  It  is  peculiar  in  the  respect  that  it  begins  a  minute  interval 
after  the  first  sound,  and  rises  in  intensity  until  it  terminates  in  the  second — 
a  systolic  crescendo  murmur,  in  marked  contrast  to  the  usual  form  of  mitral 
systolic  murmur.  I  have  watched  for  years  a  number  of  cases  who  had 
this  peculiar  murmur,  and  have  noted  that  the  majority  had  a  history  of 
rheumatism  in  their  youth,  but  I  had  no  case  that  came  to  a  post-mortem 
examination.  In  conversation  with  Dr.  David  Drummond,  he  told  me 
he  was  acquainted  with  the  murmur,  and  that  it  was  usually  associated  with 
mitral  stenosis. 

All  the  murmurs  due  to  mitral  stenosis  have  usually  a  very  limited  area 
of  propagation,  being  heard  over  a  small  space  immediately  surrounding 
the  apex  beat.  Occasionally  we  meet  with  presystolic  murmurs  heard  over 
the  whole  heart. 

§  208.  Progress  and  symptoms  in  mitral  stenosis From  the  pro- 
gressive nature  of  the  lesions  in  the  valves  and  in  the  heart  muscle,  it  will 
be  realized  that  the  symptoms  are  not  constant. 

The  patient  comes  first  into  consideration  mostly  in  early  or  middle 
adult  life.  The  complaints  then  are  shortness  of  breath,  a  sense  of  suffoca- 
tion, and  palpitation  on  exertion.     In  some  the  face  is  ruddy,  with  a  hue 


VALVULAR  DEFECTS  233 

a  shade  darker  than  is  compatible  with  the  ruddy  countenance  of  robust 
health.  At  this  stage  there  is  little  or  no  increase  in  the  size  of  the  heart 
and  no  dropsy.  A  presystolic  murmur  can  usually  be  detected.  The 
patient's  complaints  may  be  the  only  evidence  we  have  of  the  heart  failure, 
and  these  point  to  an  exhaustion  of  the  reserve  contractile  force.  After 
a  period  of  rest  this  exhaustion  may  disappear  and  the  patient  may  go  on 
for  years  with  but  little  further  trouble.  After  a  time,  however,  some 
again  break  down,  and  the  symptoms  complained  of  may  be  of  the  same 
nature.  Frequently,  however,  a  change  is  found  in  the  character  of  the 
murmurs — a  diastolic  murmur  usually  being  perceived,  and  there  is  some- 
times a  longer  duration  of  the  thrill,  these  signs  implying  an  increased  narrow- 
ing of  the  orifice.  On  the  other  hand,  in  those  in  whom  no  further  narrowing 
takes  place,  the  murmur  does  not  change,  and  the  patient  may  go  on  for 
many  years,  and,  if  a  female,  may  bear  children,  with  no  breakdown.  In 
these  cases  we  can  infer  that  there  is  no  progressive  muscular  or  valvular 
sclerosis.  With  the  increased  narrowing  of  the  orifice,  as  indicated  by  the 
appearance  of  the  diastolic  mitral  murmur,  the  heart  becomes  much  embar- 
rassed, the  symptoms  become  much  more  distressing,  and  finally  dilatation 
of  the  heart  (failure  of  tonicity)  may  set  in.  But  even  without  the  progres- 
sive narrowing,  dilatation  may  appear  early,  and  then  it  may  be  inferred 
with  certainty  that  the  rheumatic  process  has  permanently  injured  the 
heart  muscle. 

The  rhythm  of  the  heart  may  become  continuously  irregular,  from  the 
cicatrizing  process  affecting  the  a. -v.  bundle,  and  with  the  onset  of  this  nodal 
rhythm  further  embarrassment  arises  as  described  in  Chapter  XX.  If 
there  be  no  change  in  the  size  of  the  heart  with  this  nodal  rhythm,  and  no 
great  acceleration  of  rate,  the  heart  failure  may  be  very  slight  in  degree,  but 
if  the  heart  dilates,  especially  if  the  rate  is  accelerated,  then  all  the  extreme 
symptoms  of  heart  failure  follow  (dropsy,  enlargement  of  the  liver,  &c. 
See  Chapter  XX). 

In  the  vast  majority  of  cases  the  heart  recovers  from  its  first  break- 
down and  usually  from  many  subsequent  attacks.  Indeed,  after  one  attack, 
I  have  known  patients  go  on  for  twenty  years  and  more  with  no  further 
trouble  beyond  a  slight  limitation  of  the  field  of  response  to  effort. 

After  repeated  attacks,  the  patient's  life  becomes  one  of  great  limitation. 
The  future  depends  often  on  the  rapidity  of  the  advance  of  the  sclerotic 
process  of  the  valves  and  the  heart  muscle.  If  the  rate  of  advance  be  slow, 
and  the  heart  muscle  capable  of  responding  to  treatment,  the  patient  may 
go  on  for  many  years  with  a  crippled  existence.  Sometimes  we  find  in  the 
young,  about  twenty  years  of  age,  at  the  post-mortem  examination,  the 


234  DISEASES  OF  THE  HEART 

orifice  narrowed  to  a  mere  slit.  In  others  we  find  the  mitral  orifice  not  much 
contracted  but  the  heart-wall  greatly  dilated,  and  evidence  of  fibrosis  of  the 
muscle.  Hence  it  will  be  seen  that  the  progress  of  these  cases  is  largely- 
dependent  on  the  rate  of  change  in  the  muscle  as  well  as  in  the  valve.  The 
final  issue  is  usually  by  great  extension  of  the  dropsy  and  exhaustion. 

There  are  several  complications  which  may  arise. 

§  209.  Occasional  symptoms.  Paroxysmal  tachycardia. — In  place 
of  the  nodal  rhythm  being  permanently  estabHshed,  it  may  appear  inter- 
mittently as  attacks  of  paroxysmal  tachycardia.  These  attacks  are  of 
varying  importance.  Some  patients  may  have  them  for  more  than  twenty 
years  and  seem  httle  the  worse.  Others  may  have  them  occasionally,  and 
then  the  heart  settles  down  with  the  rhythm  permanently  altered.  In  such 
cases  the  future  depends  on  whether  the  heart  slows  down  or  remains 
at  a  greatly  increased  rate,  as  already  described  (§  160,  also  Case  11, 
Appendix  II). 

Haemoptysis. — At  various  stages  patients  may  be  seized  with  great 
bleeding  from  the  lungs.  Here  doubtless  the  cause  is  the  back-pressure  in 
the  pulmonary  circulation  and  rupture  of  the  blood-vessels.  As  a  rule  this 
is  a  grave  sign,  the  patient  dying  sometimes  shortly  after  an  attack. 

Cerebral  embolism. — Vegetations  may  exist  at  the  mitral  valves,  with 
no  certain  sign  of  their  presence  until  a  small  portion  is  detached  and 
impacted  in  some  vessel,  giving  rise  to  a  hemiplegic  attack,  or  an  attack  of 
aphasia.  Usually  recovery  takes  place  speedily,  and  may  be  permanent, 
but  cases  have  been  recorded  in  which  the  aphasia  or  hemiplegia  has  remained 
complete  for  many  years. 

Attacks  of  angina  pectoris. — Although  very  rare,  these  may  occur  in 
mitral  stenosis.  In  the  few  cases  I  have  observed  they  were  all  secondary 
to  some  excessive  exertion,  and  the  patients  had  only  one  or  two  attacks, 
remaining  perfectly  free  from  them  for  years  afterwards. 

Mitral  Regurgitation 

Mitral  regurgitation  may  be  the  result  of  a  damaged  valve  or  of  dilatation 
of  the  orifice  from  depression  of  the  tonicity  of  the  muscles  supporting 
the  valves. 

§  210.  Murmurs  due  to  mitral  regurgitation — The  murmur  of 
mitral  regurgitation  is  systohc  in  time,  heard  loudest  at  the  apex.  It  may 
be  soft  and  blowing,  of  little  intensity,  and  heard  over  a  very  limited  area,  or 
propagated  into  the  axilla.  Or  it  may  be  rough  and  loud,  and  heard  over 
the  whole  heart  and  round  to  the  back  of  the  chest.  It  is  not  always 
possible  to  tell  whether  it  is  due  to  dilatation  of  the  orifice  or  to  damage 


VALVULAR  DEFECTS  235 

of  the  valves.     The  rough  loud  murmur  with  an  accompanying  thrill  is 
always  a  sign  of  damaged  valves. 

§211.  Conditions  inducing  heart  failure  in  mitral  regurgitation. 
— When  the  muscle  is  unimpaired,  little  or  no  bad  effect  may  follow  damage 
to  the  mitral  valves.  Even  where  the  regurgitation  is  due  to  '  functional  ' 
dilatation  of  the  orifice  from  depressed  tonicity,  the  contractile  power  of 
the  muscle  may  maintain  a  good  and  efficient  circulation.  The  really 
serious  trouble  in  connexion  with  mitral  regurgitation  arises  when  the 
muscle  is  impaired  and  the  regurgitation  is  due  to  a  complication  of  the 
dilated  orifice  and  diseased  valve.  The  subsequent  results  depend  on  the 
degree  of  the  exhaustion  of  the  muscle  of  the  heart.  The  backward  pressure 
resulting  from  the  regurgitation  embarrasses  the  left  auricle,  pulmonary 
circulation,  and  right  heart.  The  degree  to  which  this  may  extend  depends 
in  a  great  measure  on  the  tone  of  the  heart  muscle.  While  back-pressure  is 
a  factor  of  importance  and  may  be  a  predisposing  cause,  yet  it  produces 
comparatively  few  symptoms  until  the  tonicity  gives  way,  which  is  mani- 
fested by  dilatation  of  the  heart.  The  dilatation  is  generally  looked  upon 
as  the  result  of  the  regurgitation,  the  back-pressure  ultimately  producing 
yielding  of  the  walls  of  the  right  heart.  This  is  not  quite  correct,  for  long 
before  there  is  any  back-pressure  we  may  find  evidence  of  a  dilated  right 
heart.  If  we  examine  carefully  the  condition  of  the  heart  when  the  valves 
have  been  damaged  by  rheumatic  endocarditis,  during  one  of  the  shght 
attacks  of  heart  failure  which  are  liable  to  occur  after  over-exertion,  we  may 
find  the  heart  shghtly  dilated,  the  right  ventricle  being  in  front  so  that 
the  left  ventricle  is  pushed  to  the  left  behind  the  lung  ;  the  apex  beat  is 
then  due  to  the  right  ventricle,  which  gives  a  negative  cardiogram  (Fig.  33). 
After  a  few  days'  rest  and  treatment,  the  right  heart  may  retreat  and  the 
apex  beat  is  then  due  to  the  left  ventricle,  the  cardiogram  now  presents  the 
normal  characters,  rising  during  systole.  In  such  cases  there  is  no  evidence 
whatever  of  pulmonary  engorgement  and  back-pressure.  In  fact,  in  the 
majority  of  cases,  as  Graham  Steell^^°  says,  the  change  in  the  'valves  is  alto- 
gether inadequate  to  explain  the  evidently  free  regurgitation  that  occurred 
during  life,  and  the  disastrous  dilatation  of  the  heart.  The  muscle-failure 
factor,  it  may  be  presumed,  was  the  essential  one  '. 

The  damage  to  the  valves  is  most  commonly  the  result  of  rheumatic 
endocarditis,  and,  as  we  have  seen,  the  process  is  rarely  limited  to  the 
endocardium,  but  invades  the  myocardium.  Septic  endocarditis  may  also 
damage  the  valves.  In  all  cases  of  mitral  stenosis  there  is  mitral  regurgita- 
tion, but  the  amount  of  the  regurgitation  is  never  so  marked  as  to  be  the 
serious  factor  in  the  case. 


236  DISEASES  OF  THE  HEART 

Serious  regurgitation  occurs  through  the  mitral  orifice  with  the  valves 
uninjured  in  the  latter  stages  of  many  affections,  but  more  particularly  in 
renal  disease  and  cardio-sclerosis.  Here  the  condition  is  brought  about 
by  the  failure  of  the  muscle  to  support  the  orifice,  and  this  is  too  often  the 
sign  of  a  final  and  fatal  exhaustion  of  the  heart  muscle  (see  Chapter  XXVII). 

It  will  thus  be  seen  that  the  symptoms  produced  by  mitral  incompetence 
are  only  of  gravity  when  there  is  also  muscle  failure,  and  this  is  dealt 
with  in  sufficient  detail  in  the  chapter  on  Dilatation  of  the  Heart 
(Chapter  XXIII). 


CHAPTER   XXVI 

Valvular  Defects  (continued) 

§  212.  Tricuspid  incompetence. 

213.  Tricuspid  stenosis. 

214.  Disease  of  the  aortic  valves.     Etiology. 

215.  Aortic  stenosis. 

216.  Aortic  incompetence. 

217.  Prognosis  in  valvular  affections. 

218.  Treatment. 

Affections  of  the  Tricuspid  Valves 

Lesions  of  the  tricuspid  valves  are  rare,  and  are  nearly  always 
associated  with  similar  lesions  in  the  mitral  and  aortic  valves.  The  heart 
failure  associated  with  these  lesions  is  never  due  to  the  tricuspid  lesion 
alone. 

§  212.  Tricuspid  incompetence — Although  actual  disease  of  the  valves 
is  rare,  incompetence  of  the  tricuspid  orifice  is  extremely  common — so  com- 
mon, indeed,  that  I  am  inclined  to  look  upon  the  valves  as  being  barely  able 
to  close  the  orifice  perfectly.  This  view  is  based  upon  the  observation  of 
many  patients,  in  whom  I  have  been  able  to  detect  a  tricuspid  systolic 
murmur  with  no  appreciable  increase  in  the  size  of  the  heart.  The  murmur 
in  many  cases  is  very  fugitive,  being  present  in  the  first  few  minutes  of  an 
examination,  and  disappearing  when  the  heart  becomes  quieter.  A  con- 
sideration of  the  size  of  the  orifice  and  the  size  of  the  valves  led  John 
Hunter  ^^^  to  doubt  their  competency,  while  Mayo  ^^  declared  that  the 
tricuspid  valves  never  perfectly  close  the  orifice.  Experimentally  it  has 
been  found  impossible  to  raise  the  pressure  in  the  right  ventricle,  on  account 
of  the  ease  with  which  regurgitation  takes  place  through  the  tricuspid  orifice. 

The  slighter  forms  of  tricuspid  murmurs  are  limited  to  a  small  area 
over  the  middle  of  the  sternum.  With  increase  in  the  size  of  the  right 
heart  they  may  be  heard  over  the  whole  anterior  surface  of  the  heart.  They 
are  often  associated  with  mitral  systolic  murmurs,  but  one  can  usually  detect 
a  difference  in  quality  in  the  mitral  murmur  heard  beyond  the  left  nipple 
line  and  in  the  axilla  from  the  tricuspid  murmur  heard  over  the  middle  of 
the  sternum. 

It  should  never  be  concluded  that  no  tricuspid  regurgitation  occurs 


238  DISEASES  OF  THE  HEART 

because  of  the  absence  of  a  murmur,  for  it  is  of  frequent  occurrence  to  find 
evidence  of  tricuspid  incompetence  in  the  character  of  the  jugular  and  liver 
pulsation  (ventricular  form),  and  in  the  greatly  widened  orifice  post  mortem, 
while  during  life  there  was  no  systolic  tricuspid  murmur.  A  weak  muscular 
waU  and  a  wide  orifice  may  give  rise  to  no  murmur. 

I  dwell  at  some  length  on  these  points,  not  because  the  tricuspid  regurgita- 
tion is  of  much  practical  value,  but  because  misunderstanding  of  its  symp- 
toms has  led  to  a  wrong  construction  being  put  on  the  effects  of  tricuspid 
regurgitation,  and  to  the  real  significance  of  the  ventricular  form  of  the 
venous  and  liver  pulse  being  missed.  I  have  already  pointed  out  that 
slight  regurgitation  in  a  normal  heart  would  add  to  the  accumulating  blood 
in  the  right  auricle  during  ventricular  systole,  and  would  therefore  be  a  factor 
in  the  production  of  wave  v  in  the  jugular  pulse.  Now  most  writers  overlook 
the  fact  that  a  dilating  auricle  is  interposed  between  ventricle  and  jugular, 
and  have  assumed  that  as  soon  as  tricuspid  regurgitation  takes  place  a  wave 
appears  in  the  jugular  at  the  beginning  of  ventricular  systole.  They  have 
therefore  regarded  the  ventricular  form  of  the  venous  pulse  as  only  a  sign 
of  tricuspid  regurgitation,  and  have  missed  the  real  significance  of  this 
very  important  symptom.  •  That  it  is  a  sign  of  tricuspid  regurgitation  there 
is  no  doubt,  but  it  is  a  sign  of  far  greater  significance,  namely,  that  the 
auricle  does  not  precede  the  ventricle  in  the  cardiac  cycle.  This  is  illustrated 
in  Chapter  XX  and  Appendix  II. 

§  213.  Tricuspid  stenosis. — In  the  majority  of  cases  tricuspid 
stenosis  is  not  recognized  during  life,  as  the  symptoms  produced  are  not 
always  distinctive.  It  is  only  rarely  that  a  presystoUc  tricuspid  murmur 
is  heard  ;  I  have  only  heard  it  in  three  cases,  in  which  it  was  present  in 
a  very  limited  area  over  the  middle  of  the  sternum.  There  is  usually  present 
also  a  mitral  presystoHc  murmur  at  the  apex,  but  as  each  murmur  is  con- 
fined to  such  limited  regions  I  have  had  no  difficulty  in  distinguishing  them. 
In  one  case  the  auricle  had  become  so  greatly  hypertrophied  that  it  sent 
back  a  large  wave  into  the  jugular,  and  that  with  such  force  that  it 
caused  the  valves  in  the  jugular  and  subclavian  veins  to  close  with 
a  snap,  which  I  could  hear  over  these  veins  as  a  clear,  sharp  sound 
preceding  the  first  sound. 

As  a  result  of  the  stenosis  of  the  tricuspid  orifice,  the  right  auricle  hyper- 
trophies, and  on  this  account  sends  a  wave  back  into  the  vein  Avith  such  force 
that  it  distends  the  liver,  and  I  therefore  look  upon  pulsation  of  the  fiver 
with  a  marked  wave  due  to  the  auricle  as  an  evidence  of  possible  tricuspid 
stenosis  (§  120). 

§  214.  Disease  of  the  aortic  valves.     Etiology. — By  far  the  greater 


VALVULAR  DEFECTS  239 

number  of  cases  of  affection  of  the  aortic  valves  owe  the  lesions  primarily 
to  one  of  two  conditions — rheumatic  endocarditis  and  the  sclerotic  process 
accompanying  arterial  degeneration.  Under  rare  circumstances  the  valves 
may  rupture,  but  here  there  is  usually  some  antecedent  disease  of  the  valve. 
Congenital  defects  may  in  rare  cases  give  rise  to  great  embarrassment  of  the 
heart. 

It  is  the  lesions  induced  by  the  two  first-named  conditions  that  require 
most  consideration.  In  both  instances  the  condition  is  usually  well  estab- 
lished before  it  is  found  out.  In  many  cases  the  presence  of  aortic  changes 
is  discovered  accidentally,  when  a  systematic  examination  is  being  made 
for  other  ailments,  or  for  insurance  or  a  health  certificate. 

The  heart  failure  in  aortic  valvular  disease  is  rarely  due  to  this  lesion 
alone.  In  the  majority  of  cases  changes  impairing  the  power  of  the  muscle 
have  been  proceeding  at  the  same  time  as  those  that  induced  the  valvular 
changes. 

In  the  rheumatic  cases  there  is  frequently  present  a  comphcating  lesion 
of  the  mitral  valve. 

When  the  valvular  disease  embarrasses  the  heart's  work  by  the  extent  of 
the  lesion,  as  by  great  incompetence,  and  the  heart  muscle  is  healthy,  the 
latter  responds  to  the  obstruction  to  its  work  by  hypertrophy,  and  this  may 
proceed  to  an  enormous  extent,  giving  rise  to  one  of  the  largest  of  human 
hearts — the  Cor  Bovinum. 

§  215.  Aortic  stenosis — Aortic  stenosis  is  often  associated  with  aortic 
regurgitation,  and  the  symptoms  of  the  latter  usually  dominate  the  situation. 
When  there  is  little  or  no  regurgitation,  the  symptoms  of  aortic  stenosis, 
being  less  prominent,  are  often  only  detected  accidentally  in  the  routine 
examination  of  the  patient. 

The  sign  most  characteristic  of  aortic  stenosis  is  a  murmur  systohc  in 
time,  heard  loudest  over  the  second  right  costal  cartilage,  and  propagated 
into  the  carotids.  It  may  be  faint — a  mere  whiff,  or  it  may  be  pro- 
longed, and  accompanied  by  a  thrill  perceptible  over  the  upper  part 
of  the  chest- wall.  The  heart's  rate  is  often  slow,  between  fifty  and  sixty 
beats  per  minute.  The  radial  pulse  is  sometimes  very  characteristic.  It 
impinges  against  the  finger  in  a  slow,  leisurely  fashion,  and  a  sphygmo- 
graphic  tracing  may  show  a  slanting  up-stroke  with  a  shght  interruption 
near  the  summit  (anacrotic  pulse,  Fig  145),  or  even  a  double  wave  at  the 
top  (pulsus  bisferiens.  Fig.  146).  Graham  SteelP^^  and  Lewis  ^^^  state  that 
they  have  been  able  to  detect  this  double  beat  by  the  finger,  and  Graham 
Steell  says  he  has  perceived  it  on  one  side  only.  Its  real  nature  is  yet 
obscure. 


240 


DISEASES  OF  THE  HEART 


Beyond  these  signs  there  is  Httle  that  is  characteristic  in  aortic  stenosis. 
There  may  be  symptoms  of  angina  pectoris,  but  these  are  due  to  associated 
changes  in  the  heart  muscle,  and  other  evidences  of  heart  faihire  can  be 
referred  to  the  same  cause. 

§  2i6.  Aortic  incompetence — The  aortic  valves  being  contracted  are 
no  longer  able  to  support  efficiently  the  column  of  arterial  blood  during  the 
diastole,  but  permit  a  backward  flow  into  the  heart,  and  as  a  result  we  find 
certain  alterations  in  the  character  of  the  second  sound  and  of  the  arterial 


Fig.  145.     Anacrotic  pulse,  from  a  case  of  aortic  stenosis. 

pulse.  The  closure  of  the  valves  no  longer  gives  to  the  second  sound  the 
characteristic  snap,  but  the  sound  ends  in  a  murmur  sometimes  long  drawn 
out,  sometimes  so  brief  as  to  be  scarcely  perceptible — as  if  the  second  sound 
terminated  not  abruptly  but  with  a  faint  sigh.  The  diastolic  murmur  is 
usually  propagated  down  the  sternum,  but  sometimes  it  is  heard  loudest  at 
the  apex.  Foster  has  suggested  that  this  variation  in  the  propagation  of 
the  murmur  depends  on  the  direction  given  to  the  backward  flow  by  the 


Fig.  146.     Pulsus  bisferiens,  from  a  case  of  aortic  stenosis. 


position  of  the  retracted  valve.     This  seems  plausible,  but  I  have  not  been 
able  to  verify  it,  and  the  explanation  is  ignored  in  recent  textbooks. 

The  regurgitant  murmur  is  usually  associated  with  the  murmur  of 
aortic  stenosis,  and  we  get  the  characteristic  double  aortic  murmur  (bellows 
murmur).  There  is  frequently  dilatation  of  the  smaller  arteries,  and  this, 
combined  with  the  effect  of  the  regurgitation  on  the  arterial  pulse,  causes  the 
artery  to  become  emptier  than  usual  towards  the  end  of  diastole.  This  means 
a  fall  of  pressure,  and  in  order  to  maintain  a  normal  mean  pressure  the 
heart  increases  the  force  of  its  contractions  raising  the  pressure  during 
systole,  so  that  there  is  a  great  increase  in  the  systolic  pressure  and  a  great 
fall  during  diastole,  thus  giving  rise  to  the  characteristic  collapsing  pulse 
(Corrigan's  pulse,  the  water-hammer  pulse.  Figs.  147,  148,  149).  The 
collapsing  character  of  the  radial  pulse  may  be  intensified  by  raising  the 


VALVULAR  DEFECTS  241 

arm  above  the  head.  At  times  the  arterial  pulse  is  conveyed  through  the 
capillaries  into  the  veins,  and  G.  Gibson  has  obtained  a  graphic  record  of 
such  pulsation  of  the  veins  on  the  back  of  the  hand.  If  the  forehead  be 
rubbed  so  as  to  produce  redness,  the  flush  is  seen  to  wax  and  wane  with 
each  beat  of  the  heart  (capillary  pulsation). 


Fig.  147.     Pulse  of  slight  aortic  regurgitation  with  good  heart  muscle. 

The  double  aortic  murmur  may  be  detected  without  any  history  of  a 
heart  affection.  In  many  cases  there  may  be  little  or  no  dilatation,  and  the 
individual  may  be  able  to  indulge  in  games  and  in  occupations  requiring 
considerable  exertion  with  no  discomfort.     In  such  cases  it  may  safely  be 


Fig.  148.     Pulse  of  slight  aortic  regurgitation  with  gi-eat  cardiac  failure. 

assumed  that  the  damage  to  the  valves  has  been  slight,  and  that  the  heart 
muscle  has  escaped  serious  injury. 

In  other  cases  the  heart  is  greatly  enlarged  and  the  apex  beat  is  diffuse 
and  forcible.    The  systole  and  diastole  of  the  heart  may  cause  movements 


Fig.  149.     Pulse  of  extreme  aortic  regurgitation  with  great  cardiac  failure. 

of  the  liver  that  simulate  pulsation  of  that  organ,  but  analysis  of  its  graphic 
records  show  it  to  be  merely  the  dragging  up  and  pushing  down  of  the  liver 
by  the  changes  in  the  size  of  the  heart  (Figs.  27,  28).  Even  under  these 
circumstances  the  individual  may  for  years  pursue  an  active  vocation,  but 
he  is  always  liable  to  attacks  of  heart  failure.  The  condition  is  often 
associated  with  affection  of  the  mitral  valves,  and  this  is  one  of  the  factors 


MACKENZIE 


242  DISEASES  OF  THE  HEART 

participating  in  the  production  of  the  heart  failure  that  finally  terminates 
these  cases. 

The  most  frequent  sufferers  from  aortic  valvular  disease  are  the  middle- 
aged.  In  them  the  sclerotic  process  has  been  gradually  advancing,  and  the 
early  symptoms  of  exhausted  reserve  force  have  been  neglected  until  symp- 
toms of  distress  command  attention.  There  may  have  been  a  history  of 
rheumatism,  of  excessive  drinking,  of  hard  bodily  exertion,  of  syphihs,  but, 
on  the  other  hand,  no  definite  causal  condition  may  be  discovered.  The 
facial  aspect  is  frequently  pale  grey  (earthy  countenance),  though  in  others 
it  may  be  full-blooded  and  ruddy.  The  complaints  are  varied.  Shortness 
of  breath  on  exertion,  violent  throbbing  in  the  neck,  attacks  of  pain  over 
the  chest  on  exertion,  are  amongst  the  most  common  symptoms  of  which 
the  patient  complains  in  the  first  instance.  For  a  varying  period,  under 
suitable  treatment,  a  certain  store  of  reserve  force  is  gained,  and  he  may  go 
on  for  months  or  years,  sometimes  in  fair  comfort,  but  his  existence  is  usually 
more  or  less  crippled. 

The  end  of  these  patients  is  frequently  dilatation  of  the  heart,  dropsy, 
and  exhaustion.  Sometimes  this  is  due  to  the  inception  of  the  nodal  rhythm. 
Those  who  suffer  from  angina  pectoris  may  die  suddenly.  I  have  seen  a  few 
cases  die  during  a  sudden  attack  of  dyspnoea  of  the  greatest  severity. 

§  217.  Prognosis  in  valvular  affections — The  heart  failure  depends 
upon  so  many  and  so  varied  conditions — as  the  extent  of  the  valvular  lesion, 
its  progressive  nature  depending  on  the  cicatrizing  process  affecting  the 
valves,  the  coincident  changes  in  the  muscle  and  in  the  a. -v.  bundle,  the 
conditions  of  life  of  the  individual — that  no  rule  applicable  to  aU  cases  can 
be  made.  If,  however,  an  attempt  be  made  to  appreciate  the  value  of  the 
symptoms  present,  on  the  lines  I  have  laid  down,  an  approach  to  a  true 
prognosis  may  be  made  in  each  case.  There  is  just  one  point  I  again  wish 
to  insist  upon  :  let  no  single  symptom  be  the  ground  for  forming  a  prognosis. 
In  this  respect  the  presence  of  a  murmur  has  so  oppressed  the  profession  that 
a  vast  amount  of  positive  harm  is  continually  being  done  to  patients  by 
taking  too  seriously  the  prognostic  significance  of  this  sign.  The  field  of 
cardiac  response  is  the  only  true  and  safe  guide  in  these  cases.  Even  if  for 
the  time  being  it  is  limited,  judgement  should  be  suspended  until  an  oppor- 
tunity has  been  obtained  for  ascertaining  to  what  extent  the  heart  muscle 
can  regain  a  store  of  reserve  force  (see  Chapter  XXXII). 

§  218.  Treatment. — As  heart  failure  with  valvular  defects  touches 
every  phase  of  the  subject,  the  matter  of  treatment  must  be  discussed  from 
a  very  wide  aspect.  The  special  chapters  on  treatment  therefore  include 
the  full  consideration  of  this  subject. 


CHAPTER   XXVII 

Cardio-Sclerosis  (Arterial  Degeneration,     The  Senile  Heart) 

§  219.  Conditions  producing  cardio-sclerosis. 

220.  Conditions  inducing  degenerative  changes  in  the  arterial  system. 

221.  Obliteration  of  the  capillaries. 

222.  Symptoms  of  cardio-sclerosis. 

223.  Prognosis. 

224.  Treatment. 

225.  Aneurysm. 

§  219.  Conditions  producing  cardio-sclerosis.  There  are  certain 
changes  which  we  recognize  as  accompanying  and  giving  rise  to  the  features 
characteristic  of  advancing  years.  These  changes  may  be  detected  in  every 
tissue  and  organ  of  the  body,  and  they  can  be  recognized  in  the  bald  scalp, 
white  hair,  or  tortuous  artery.  The  changes  in  the  arteries  and  capillaries 
may  modify  the  structure  and  functions  of  the  various  organs,  but  not  all 
organs  equally.  Arterial  degeneration  may  in  one  person  be  more  advanced 
in  the  brain,  in  another  in  the  kidneys,  in  another  in  the  limbs,  in  another 
in  the  heart.  In  many  these  changes  are  merely  those  associated  with 
advancing  years,  and  give  rise  to  what  we  understand  by  senile  changes. 
When  affecting  the  heart  they  are  usually  accompanied  by  some  fibrous  or 
fatty  changes  in  the  heart  muscle.  If  these  changes  are  considerable  in 
extent,  then  we  get  a  train  of  symptoms  which  we  recognize  as  due  to 
'  cardio-sclerosis  '. 

There  are  two  main  circumstances  that  induce  degenerative  changes 
(fatty  and  fibrous)  in  the  heart,  namely,  the  cicatricial  changes  that  follow 
acute  affections,  as  after  rheumatic  fever,  and  the  changes  that  accompany 
arterial  degeneration.  Both  these  conditions  affect  the  muscular  structure 
as  well  as  the  valves,  and  the  resulting  heart  failure  is  often  the  outcome 
of  the  invasion  of  both  tissues  by  the  sclerotic  process.  Although  it  may  be 
convenient  to  follow  conventional  lines  and  describe  separately  the  valvular 
affections,  it  must  be  borne  in  mind  always  that  in  the  serious  cases  there 
is  a  widespread  condition  of  which  the  valvular  lesion  is  but  a  part. 

The  changes  in  cardio-sclerosis  due  to  rheumatic  fever  have  a  certain 
resemblance  to  those  due  to  arterial  degeneration.  In  both  instances  there 
is  a  replacement  of  the  muscular  fibres  by  fibrous  tissue,  and  a  shrinking 

R  2 


244  DISEASES  OF  THE  HEART 

of  the  valvular  apparatus,  and  as  a  consequence  both  conditions  present 
identical  symptoms.  Though  there  is  this  resemblance  in  progress  and 
symptoms,  there  are  other  differences  which  have  an  important  bearing  on 
prognosis  and  treatment. 

The  consideration  of  the  rheumatic  and  other  inflammatory  forms  of 
sclerosis  is  included  in  the  chapters  on  valvular  disease.  Here  I  wish  to 
draw  particular  attention  to  the  changes  in  the  heart  that  are  associated 
with  arterial  degeneration  and  senile  changes.  The  causes  of  arterial 
degeneration  are  still  not  clear,  and  it  is  difficult  to  say,  of  the  complications 
in  any  given  case  showing  arterial  degeneration,  which  are  the  cause  and 
which  the  consequence.  Clifford  Allbutt  ^^  rightly  protests  against  arterio- 
sclerosis being  considered  a  disease  ;  it  is  the  outcome  of  processes  which 
we  imperfectly  understand,  and  may  arise  as  the  result  of  high  blood-pressure, 
toxic  conditions,  or  senile  changes.  I  do  not  enter  into  the,  at  present, 
hopeless  task  of  distinguishing  the  causes  of  the  changes  in  the  arterial 
system.  A  little  of  the  truth  may  be  present  in  each  of  the  many  competing 
theories  at  present  holding  the  field,  but  no  one  of  them  can  be  considered 
wholly  satisfactory  and  convincing. 

In  the  meantime,  an  appreciation  of  the  changes  as  they  affect  the  heart 
gives  us  great  assistance  in  the  treatment  of  our  patients. 

§  220.  Conditions  inducing  degenerative  changes  in  the  arterial 
system. — It  is  usual  to  attribute  the  changes  to  some  earlier  process  that 
has  affected  the  blood  or  the  arteries,  of  which  kidney  disease,  sj^hilis,  over- 
exertion, are  the  most  striking  examples.  But  it  wiU  be  found  frequently 
that  extensive  arterial  degeneration  may  be  present  for  which  one  can 
find  no  definite  cause. 

There  can  be  no  doubt  that  affections  of  the  kidneys  tend  to  induce  these 
changes.  But  in  many  people  the  kidney  lesions  are  undoubtedly  secondary, 
and  patients  may  show  well-marked  and  extensive  arterial  degeneration 
many  years  before  there  is  the  slightest  evidence  of  kidney  ailment.  In 
such  instances  it  is  but  reasonable  to  assume  that  the  renal  degeneration, 
like  the  cardiac  and  cerebral,  is  secondary  to  the  arterial  degeneration. 

§  221.  Obliteration  of  the  capillaries One   of   the   most   striking 

changes  that  take  place  in  the  progress  of  arterial  degeneration  is  the 
diminution  of  the  capillary  field.  This  obliteration  of  the  capillaries  is 
likely  to  be  found  of  the  greatest  importance  not  only  in  the  production  of 
the  degenerative  changes  that  occur  in  the  heart  itself,  but  by  narrowing 
the  communication  between  the  arterial  and  the  venous  system  it  entails 
more  work  on  the  heart  in  forcing  the  blood  through  the  constricted  area. 

If  one  notes  the  changes  in  the  skin  that  occur  with  advancing  years. 


CARDIO-SCLEROSIS  246 

how  it  loses  its  velvety  thickness,  becomes  shrivelled  and  attenuated,  so 
that  in  advanced  conditions  the  scalp  may  be  found  denuded  of  hair  and 
plastered  to  the  underlying  bones,  the  extent  of  the  diminution  of  the  capil- 
lary field  may,  to  a  certain  extent,  be  appreciated.  A  still  more  striking 
evidence  of  the  diminished  capillary  field  in  the  old  is  the  absence  of  free 
bleeding  in  a  freshly-made  wound.  In  the  young  the  abundant  oozing  of 
bright  red  blood  is  a  source  of  satisfaction  to  the  surgeon,  for  it  is  a  testimony 
to  the  healthiness  of  the  subject  and  to  the  recuperative  power,  and  is  in 
striking  contrast  to  the  bleeding  from  a  wound  in  the  aged,  where  the  bleeding 
is  mostly  from  some  cut  vein  or  from  the  persistent  spouting  of  a  degenerated 
artery,  indicating  an  impoverished  blood-supply  rendering  the  healing 
process  less  satisfactory. 

This  diminution  of  the  capillary  field,  so  easily  recognized  in  the  external 
body-wall,  also  occurs  in  the  heart,  and  the  results  are  shown  in  a  variety 
of  ways.  It  leads  to  malnutrition  of  the  tissues  and  degeneration  of  the 
heart  muscle.  The  character  of  the  degeneration  varies  according  to  the 
structure  affected,  but  in  all  it  leads  to  impairment  of  function.  The  first 
structures  to  show  evidence  of  the  capillary  obliteration  are  those  that  have 
the  smallest  blood-supply,  and  it  may  be  partly  for  this  reason  that  it  is 
early  marked  in  the  cornea  (arcus  senilis),  the  valves  of  the  heart,  and  the 
arterial  walls. 

In  the  heart  muscle  the  effect  of  these  changes  in  the  arteries  and 
capillaries  is  a  degeneration,  fibrous  or  fatty.  In  the  production  of  this 
myocardial  degeneration  we  get  the  diminished  capillary  field  complicating  the 
consequences  of  the  degenerated  artery — a  degeneration  at  times  so  extreme 
that  little  blood  can  penetrate  the  coronary  arteries  or  their  branches.  If  it 
be  borne  in  mind  how  dependent  the  muscular  structure  of  the  heart  is  upon 
an  abundant  supply  of  blood,  it  will  be  easy  to  recognize  the  fact  that  such 
changes  must  have  a  profound  effect  upon  the  efficiency  of  the  organ. 

Accompanying  the  arterial  degeneration,  Savill*^^  and  Russell  *^^  have 
shown  a  great  increase  in  the  muscular  coat  of  the  smaller  arteries.  This 
hypertrophy  implies  during  life  abnormal  contraction  (hypertonus  of  Russell). 
This  is  bound  to  raise  the  blood-pressure  and  embarrass  the  heart. 

The  diminished  capillary  field  has  also  probably  a  further  complicating 
effect  in  so  far  as  it  introduces  an  obstruction  to  the  heart's  contraction. 
The  narrowing  of  the  outflow  necessitates  a  greater  force  to  send  the  blood 
through  the  tissues  ;  consequently  the  ventricle  has  to  contract  more  strongly 
to  raise  the  arterial  pressure,  and  thus  produces  a  further  embarrassment  to 
the  degenerated  heart. 

§  222.  Symptoms  of  cardio-sclerosis. — The  symptoms  arising  from 


246  DISEASES  OF  THE  HEART 

such  changes  are  extremely  varied,  ^nd  at  first  sight  hopelessly  confused,  but 
there  is  good  reason  to  expect  that  with  a  better  knowledge  of  the  functions 
of  the  different  parts  of  the  heart  a  more  satisfactory  appreciation  of  all 
the  symptoms  may  be  obtained,  and,  in  turn,  a  more  accurate  under- 
standing of  the  symptoms  during  life  will  guide  the  pathologist  in  his  post- 
mortem examination.  I  have  submitted  to  Professor  Keith  a  large  number 
of  hearts  afEected  by  the  changes  associated  with  arterio-sclerosis  from 
patients  ranging  from  forty-two  to  seventy-seven  years  of  age,  and  in  all  the 
post-mortem  appearance  had  such  a  close  resemblance  that  it  might  have 
been  assumed  that  during  Ufe  the  sjnmptoms  would  have  been  identical. 
A  study  of  these  symptoms  showed,  however,  a  wide  diversity,  soine  patients 
suffering  from  angina  pectoris,  others  with  no  pain  ;  some  with  severe 
cardiac  asthma,  others  with  no  respiratory  trouble  ;  some  had  very  irregular 
hearts,  others  frequent  or  infrequent  extra-systole,  while  some  had  marked 
pulsus  alternans,  and  in  others  the  heart  was  perfectly  regular  till  the  end. 
Some  patients  had  extensive  dropsy,  other  patients  showed  no  sign  of 
oedema.  Some  had  aortic  or  mitral  murmurs,  others  had  no  murmurs.  It 
will  thus  be  seen  that  the  symptoms  of  well-authenticated  cardio-sclerosis 
exhibit  every  phase  of  cardiac  symptoms,  and  the  superficial  observer  might 
think  that  each  case  presented  a  different  form  of  heart  disease.  Instead 
of  this,  while  the  organic  or  fundamental  lesion  is  the  same,  the  variety 
of  symptoms  is  due  to  the  different  parts  or  functions  particularly  affected. 
The  earhest  result  of  cardio-sclerosis  is  a  diminution  of  the  reserve  force 
of  the  heart,  manifested  by  a  hmitation  of  the  field  of  cardiac  response.  The 
patient  rarely  presents  himself  before  the  physician  until  this  exhaustion  of 
the  reserve  force  has  produced  some  distressing  symptom,  it  may  be  breath- 
lessness,  cardiac  asthma,  angina  pectoris,  or  '  bronchitis  '.  In  every  case 
it  will  be  found  to  be  preceded  by  a  history  of  an  ever-diminishing  area  of 
cardiac  response.  At  the  beginning  the  individual  will  not  acknowledge 
that  his  powers  are  being  curtailed — indeed  the  patient  may  be  proud  of  his 
virility — but  it  may  be  taken  as  a  certain  sign  that  when  a  middle-aged  man 
boasts  of  his  strength  he  is  trying  to  hide  from  others  his  own  consciousness 
of  a  limitation  of  his  powers.  Continuing  to  work  as  hard  as  he  did  before 
these  degenerative  changes  made  their  appearance,  the  exliaustion  of  the 
reserve  force,  though  slight  at  first  and  scarcely  perceptible,  in  the  long  run 
reaches  a  stage  when  the  suffering  or  discomfort  entailed  compels  the  patient 
to  consult  his  physician.  When  this  occurs  the  changes  in  heart  and  blood- 
vessels are  well  estabfished.  The  skin  of  the  hand  has  already  lost  its  velvety 
thickness,  and  the  arteries  show  a  varying  degree  of  change,  as  tortuosity, 
slight  or  considerable  thickening  of  the  radial  ;    sometimes  one  can  detect 


CARDIO-SCfiEROSIS  247 

pieces  of  peculiar  hardness,  fine  and  granular,  or  patches  Uke  small  beads, 
or  the  artery  may  be  thickened  Uke  the  characteristic  pipe-stem,  the  surface 
being  shghtly  nodulated. 

Even  in  the  absence  of  any  of  these  signs  in  the  superficial  arteries,  it 
must  not  be  inferred  that  the  degenerative  process  is  absent  in  the  visceral 
arteries.  Arterial  degeneration  is  often  very  irregularly  distributed,  affecting 
different  regions  in  different  patients.  It  is  for  this  reason  that  in  this  affec- 
tion the  symptoms  of  its  progress  may  be  more  marked,  now  in  the  cerebral 
arteries,  giving  rise  to  cerebral  apoplexy,  now  in  the  arteries  of  the  leg,  giving 
rise  to  gangrene,  now  in  the  arteries  of  the  heart,  giving  rise  to  the  symptoms 
here  described. 

The  blood-pressure  measurements  show,  in  many  cases,  a  great  rise.  In 
the  earlier  stages,  when  the  patients  are  first  seen,  there  is  seldom  much 
enlargement  of  the  heart  unless  there  has  been  long-standing  Bright 's  disease. 
Usually  the  heart's  dullness  does  not  extend  beyond  the  nipple  fine.  The 
sounds  of  the  heart  may  be  clear  and  well  struck,  often  with  some  accentua- 
tion of  the  second  sound.  In  some  an  aortic  murmur  may  be  present,  most 
frequently  systoHc  in  time,  though  occasionally  there  may  also  be  a  diastohc 
murmur,  usually  of  very  short  duration.  The  heart's  action,  though  fre- 
quently perfectly  regular  until  the  end,  may  show  irregularities,  the  most 
common  being  of  the  nature  of  extra-systole.  In  advanced  cases  we  may 
find  good  examples  of  the  pulsus  alternans.  The  heart  may  be  continuously 
irregular  (nodal  rhythm),  and  sometimes  of  great  rapidity.  Not  infrequently 
this  continuous  irregularity,  with  or  without  excessive  rapidity,  comes  on  in 
intermittent  attacks  lasting  for  a  few  minutes,  a  few  hours,  or  a  few  days 
(paroxysmal  tachycardia).  In  rare  cases  the  degenerative  process  may 
affect  the  a. -v.  bundle  and  give  rise  to  heart-block. 

The  subjective  phenomena  vary.  In  the  early  stages  there  may  be  no 
symptom  beyond  a  limitation  of  the  field  of  cardiac  response,  shown  by 
breathlessness  on  moderate  exertion.  In  more  advanced  cases  there  may  be 
a  shght  tightness  across  the  chest  on  exertion  or  on  going  into  the  cold  air, 
as  on  going  from  a  warm  room  into  a  cold  bedroom,  or  going  into  the  open 
air  on  a  winter's  morning.  This  sensation  is  usually  ignored  until  it  is  accom- 
panied by  pain,  sometimes  of  such  severity  as  to  be  recognized  as  an  attack 
of  angina  pectoris.  In  rare  cases  the  pain  may  never  arise,  but  the  gripping 
sensation  felt  in  the  chest  may  be  so  severe  that  the  patient  feels  his  chest 
fixed,  and  has  to  stop  and  draw  several  deep  breaths  to  reheve  the  spasm. 

In  many  cases  it  is  only  breathlessness  on  exertion  that  arrests  the  patient, 
the  breathing  being  short  and  hurried  on  such  exertion  as  he  used  to  under- 
take in  comifort.     In  extreme  cases  the  mere  turning  over  in  bed  induces 


248  DISEASES  OF  THE  HEART 

the  hurried  respiration.     The  breathlessness  may  seize  him  in  the  night  — 
in  attacks  of  cardiac  asthma,  or  Cheyne-Stokes  respiration  may  appear. 

The  symptoms  described  so  far  arise  from  the  heart  while  the  tonicity 
is  still  good.  In  a  great  many  of  these  cases  a  stage  is  reached  when  the 
heart  dilates.  In  addition  to  the  increased  size  of  the  heart,  a  number  of 
symptoms  disappear,  while  others  come  into  prominence  ;  the  arterial 
pressure  falls,  the  attacks  of  angina  pectoris,  cardiac  asthma,  and  Cheyne- 
Stokes  respiration  usually  disappear,  while  a  mitral  systolic  murmur  may 
be  heard  ;  dropsy  sets  in,  and  oedema  of  the  lungs,  sometimes  with  the 
expectoration  of  blood,  or  blood-stained  sputa — in  short,  all  the  symptoms 
already  described  under  failure  of  tonicity  (Chapter  XXIII). 

If  the  cause  of  the  symptoms  in  cardio-sclerosis  is  appreciated,  it  helps 
one  to  understand  the  reason  of  the  great  variety  of  phenomena  present  in 
this  affection.  The  variations  in  symptoms  are  in  all  likelihood  due  to  the 
parts  invaded  by  the  degenerative  process.  As  the  presence  or  absence  of 
aortic  murmurs  depends  on  whether  the  disease  affects  the  aortic  valves,  so 
the  presence  or  absence  of  the  various  irregularities  (with  the  exception  of 
the  pulsus  altemans)  depends  on  the  invasion  of  the  primitive  cardiac 
tissue.  The  extent  of  the  invasion  determines  whether  the  irregularity  is 
limited  to  an  occasional  extra-systole,  or  whether  it  terminates  in  the  nodal 
rhythm  or  in  heart-block.  In  like  manner  the  degree  of  exhaustion  of 
the  function  of  contractiUty  determines  the  nature  of  the  subjective  pheno- 
mena, the  breathlessness,  anginal  symptoms,  and  the  cardiac  asthma.  On 
the  other  hand,  with  exhaustion  of  the  tonicity  we  get  the  transformation 
in  the  character  of  the  symptoms  resulting  in  the  dilatation  of  the  heart, 
dropsy,  oedema  of  the  lungs,  and  so  forth. 

§  223.  Prognosis — The  prognosis  depends  to  a  great  extent  on  the 
nature  of  the  symptoms,  and  the  manner  in  which  the  heart  responds  to  treat- 
ment. If,  for  instance,  a  patient  has  an  irregular  pulse  due  to  extra-systole, 
while  in  other  respects  the  response  of  the  heart  to  effort  is  such  as  woidd  be 
expected  under  normal  conditions  at  his  time  of  life,  then  the  prognosis,  in 
the  absence  of  other  evidences  of  disease,  is  very  favourable.  When  graver 
symptoms  are  present,  as  the  tightness  across  the  chest,  slight  or  severe 
attacks  of  pain,  then,  if  the  previous  history  of  the  patient  points  to  worry, 
sleeplessness,  and  overwork,  a  prognosis  should  be  deferred  to  see  how  he 
responds  to  treatment.  If  these  signs  speedily  disappear  under  treatment, 
the  prognosis  is  favourable  ;  on  the  other  hand,  the  prognosis  becomes  the 
more  unfavourable  the  more  the  symptoms  refuse  to  yield.  But  even  here 
comparative  freedom  from  suffering  may  be  enjoyed  by  a  patient  who  pursues 
a  life  that  exposes  him  to  little  effort,  and  many  patients  may  live  a  useful 


CARDIO-SCLEROSIS  249 

though  crippled  life  for  years.  Where  there  are  attacks  of  cardiac  asthma 
occurring  in  the  night,  or  attacks  of  Cheyne-Stokes  respiration,  or  when  the 
pulsus  alternans  is  present,  the  condition  may  be  considered  far  advanced, 
and  though  the  patient  may  live  for  months  or  a  few  years,  it  is  with  very 
limited  powers,  and  he  is  liable  to  a  serious  breakdown  at  any  time.  When 
the  pulse  is  continually  irregular,  the  prognosis  depends  on  how  well  the  heart 
maintains  the  circulation.  If  dropsy  supervenes  and  steadily  increases,  it  is 
not  very  susceptible  to  treatment  in  contrast  to  the  parallel  condition  due 
to  rheumatic  sclerosis.  But  apart  from  this,  many  patients  may  lead  a 
fairly  active  existence  with  the  nodal  rhythm  for  many  years,  though 
exposed  to  frequent  attacks  of  '  bronchitis  '. 

It  must  be  borne  in  mind  that  the  sudden  inception  of  the  nodal  rhythm 
is  not  infrequently  the  direct  cause  of  death  in  elderly  cardio-sclerotics. 

The  rather  rapid  dilatation  of  the  heart,  with  accompanying  dropsy,  is 
usually  a  sign  of  approaching  dissolution. 

I  doubt  if  the  blood-pressure  measurements  prove  of  much  use  as  a  guide 
in  prognosis.  I  have  watched  for  a  number  of  years  individuals  glide  past 
seventy  years  of  age  with  a  blood-pressure  from  180  to  200  mm.  Hg.,  and 
I  could  not  see  that  their  condition  was  materially  worse  in  consequence. 

§  224.  Treatment. — In  treating  cardio-sclerosis  it  should  always  be 
borne  in  mind  that  the  condition  is  progressive,  and  we  cannot  stay  it, 
because  the  changes  are  those  which  are  inseparable  from  advancing  years. 
It  usually  proceeds  very  slowly,  so  that  a  man  may  show  signs  of  arterial 
degeneration  and  irregularity  of  the  heart  from  the  age  of  fifty  to  sixty  years, 
but  may  live  in  fair  health  for  twenty  years  afterwards,  ending  his  days 
without  any  marked  failure  of  the  heart.  The  early  stages  are  generally 
recognized  in  the  examination  of  the  patient  for  some  other  condition,  when 
the  distinctive  signs  may  be  found  in  the  tortuous  arteries,  raised  blood- 
pressure,  and  the  occasional  occurrence  of  an  extra-systole.  Medical  men 
often  attempt  to  combat  these  signs  by  some  treatment  more  or  less  energetic, 
and  as  many  people  are  frightened  by  the  evidences  of  advancing  years  they 
readily  comply  with  the  proposals  that  are  supposed  to  put  back  the  hands 
of  time  ;  hence  the  great  variety  of  drugs,  methods,  and  modes  of  life  we 
find  current. 

It  is  rare  that  one  has  occasion  to  treat  the  milder  symptoms  in  the 
working-man — not  that  they  are  not  frequently  present,  but  because  he  has 
not  the  time  to  consider  his  complaints,  and  he  seems  in  no  way  to  suffer 
from  the  neglect.  It  is  the  well-to-do  who  are  most  concerned  about  some 
trifling  symptom  incidental  to  these  changes,  and  when  their  attention  is 
called  to  such  a  symptom  as  an  extra-systole,  either  by  their  own  sensations 


250  DISEASES  OF  THE  HEART 

or  by  their  medical  attendant,  they  beHeve  that  some  calamity  is  impending, 
and  readily  submit  to  any  suggestion  that  promises  to  stave  off  the  evil  day. 

When  the  patient  is  aware  of  the  irregular  action  of  his  heart,  and  when 
we  find  by  examination  that  there  are  no  changes  beyond  what  would  be 
expected  at  his  time  of  life,  he  should  be  strongly  reassured  that  the  irregu- 
larity is  a  trivial  symptom  and  of  no  vital  importance.  When  the  symptoms 
are  unpleasant  and  are  aggravated  by  his  mode  of  life — for  example,  by  too 
close  application  to  a  sedentary  occupation — certain  rational  suggestions 
as  to  the  manner  of  living  are  obligatory. 

In  cases  presenting  these  milder  signs  no  further  treatment  is  necessary, 
beyond  insisting  that  the  patient  should  lead  a  well-regulated  life,  avoiding 
over-feeding,  over-drinking,  and  taking  as  much  exercise  in  the  open  air  as 
can  be  reasonably  obtained.  Some  of  the  symptoms,  as  extra-systole,  come 
on  for  periods  and  disappear  for  longer  and  shorter  intervals.  In  these  cases 
I  have  frequently  seen  the  patient  get  much  benefit  from  a  hohday  with 
healthy  open-air  exercise.  Several  of  my  patients,  for  instance,  were  conscious 
of  the  occurrence  of  extra-systoles,  and  when  they  felt  them  they  indulged 
in  a  game  of  goK  two  or  three  afternoons  a  week,  or  took  a  short  golfing 
holiday,  and  invariably  experienced  relief.  In  fike  manner,  judicious  hill- 
climbing  and  walking  are  of  benefit.  In  some  cases  the  bodily  exertion  may 
in  the  first  instance  increase  the  frequency  of  these  extra-systoles,  but  the 
exercise  should  not  be  given  up  on  that  account ;  rather  should  it  be  continued 
with  moderation  till  a  recovery  of  the  reserve  force  takes  place  by  training, 
when  the  irregularities  wiU  become  less  frequent  or  disappear. 

The  amount  of  recovery  depends  on  the  stage  which  the  degeneration 
of  the  heart  muscle  has  reached.  We  know  of  no  method  which  can  restore 
a  better  blood-supply  by  removing  the  arterial  degeneration,  and  without 
this  it  is  impossible  to  arrive  at  any  process  that  would  restore  the  degenerated 
muscle  of  the  heart ;  so  that  when  a  considerable  degree  of  recovery  has  taken 
place,  it  is  foolish  to  imagine  that  the  favourable  result  has  come  to  pass 
because  the  treatment  has  restored  the  degenerated  muscle-fibres.  All  we 
can  say  in  such  cases  is  that  the  treatment  has  increased  the  reserve  force  of 
the  muscle-fibres.  Recovery  means  the  retention  of  a  certain  amount  of 
active  muscle-fibre,  and  the  greater  the  recoveryj^the  less  the  degeneration, 
and  the  less  serious  the  prospect  for  the  patient. 

Another  most  important  factor  in  treatment  in  all  these  cases  is  sleep. 
Many  suffer  from  troubled  and  broken  sleep,  and  when  they  begin  to  suffer 
from  attacks  of  heart  failure  the  occurrence  of  sleepless  nights  almost  invari- 
ably precipitates  the  exhaustion.  Attacks  of  angina  pectoris  may  be  directly 
induced  by  this  want  of  refreshing  sleep,  and  may  be  stopped  by  measures 


CARDIO-SCLEROSIS  251 

taken  to  induce  sleep.  The  means  best  adapted  to  this  object  varies  with 
different  individuals.  In  some  it  may  be  found  that  their  former  habits  in 
the  matter  of  their  food  are  no  longer  suitable  for  their  condition  ;  it  is  some- 
times enough  for  them  to  take  some  light  nourishment,  as  milk  or  biscuit,  on 
going  to  bed  or  during  the  night,  to  induce  a  restful  sleep.  Most  require  some 
form  of  hypnotic,  and  the  bromides — 20  grains  thrice  daily,  for  instance — 
may  induce  a  degree  of  drowsiness  that  is  very  beneficial.  Again,  the  safer 
hypnotics,  as  veronal  or  sulphonal,  prove  very  useful  in  the  milder  cases. 
When,  however,  the  nights  are  disturbed  by  attacks  of  distressful  breathing, 
oxygen  is  of  great  service  in  some  cases,  and  in  others  opiates  or  chloral  must 
be  resorted  to.  On  the  whole,  I  find  chloral  the  more  useful  drug.  But 
the  cases  are  so  variable  that  sometimes  one  drug  is  more  efficacious  than 
the  other,  so  that  it  may  be  necessary  to  try  each  of  them,  or  a  combination 
of  both.  As  regards  contra-indications,  I  do  not  prescribe  opiates  when 
there  is  exudation  in  the  bronchial  tubes  with  duskiness  of  the  face,  as  I  have 
seen  serious  results  follow,  probably  from  the  secretion  not  being  got  rid  of 
and  thus  inducing  a  certain  amount  of  suffocation,  which  further  impairs 
the  enfeebled  heart. 

Iodide  of  potassium  is  now  generally  recognized  as  of  service  in  the 
relief  of  many  of  the  milder  symptoms  associated  with  arterial  degenera- 
tion. In  many  people  the  symptoms  are  not  constant,  but  are  manifested 
occasionally  in  attacks  of  dizziness,  dull  headaches,  inabihty  to  walk  as  far 
as  usual  on  account  of  breathlessness,  sHght  attacks  of  angina  pectoris,  and 
even  more  violent  attacks  ;  these  all  seem  to  benefit  by  the  use  of  iodide 
of  potassium.  In  the  attacks  of  '  bronchitis  '  so  common  in  the  winter  and 
spring  months  in  certain  classes  I  have  found  distinct  benefits  from  the  use 
of  the  iodide.  I  am  not  at  all  sure  that  the  good  results  attributed  to  the 
iodide  may  not  have  been  due  to  the  accompanying  change  in  the  food  and 
mode  of  Hfe.     The  action  of  iodide  of  potassium  is  not  understood. 

When  dilatation  of  the  heart  sets  in,  with  dropsy  and  scanty  urine,  the 
treatment  should  follow  the  lines  laid  down  in  Chapter  XXXIII.  I  may 
remark  here  that  drugs  of  the  digitahs  group  are  frequently  of  Httle  avail  in 
these  cases.  They  may  increase  the  fiow  of  urine,  but  the  heart  does  not 
readily  respond  to  them. 

§  225.  Aneurysm — It  is  not  my  purpose  to  enter  into  the  discussion  of 
aneurysm,  as  it  comes  within  the  province  of  arterial  disease,  with  which 
I  do  not  propose  to  deal.  As,  however,  aneurysm  is  a  frequent  comphcation 
of  cardio-sclerosis  and  adds  to  the  embarrassment  of  the  heart  in  its  work, 
I  wish  to  point  out  that  many  of  the  symptoms  present  in  aneurysm  really 
arise  from  the  heart,  which  has  become  affected  by  the  processes  that  have 


252  DISEASES  OF  THE  HEART 

led  to  the  production  of  the  aneurysm.  The  aneurysm  itself  is  such  a  patent 
abnormality,  while  the  heart  affection  (cardio-sclerosis)  may  give  rise  to  no 
distinctive  sign,  that  the  cardiac  symptoms  are  usually  attributed  to  the 
aneurysm.  Thus  the  pain  in  aneurysm  is  very  often  cardiac  in  origin, 
especially  when  it  occupies  the  region  illustrated  in  Fig.  12.  There  are, 
however,  other  pains  in  aneurysm  whose  origin  it  is  difficult  to  indicate, 
such  as  the  persistent  boring  pain  felt  at  the  back  over  the  left  scapula,  or  on 
the  top  of  the  shoulder.  Whether  they  are  the  direct  result  of  the  pressure 
on  sensitive  structures,  or  are  of  the  nature  of  referred  pain,  I  cannot  decide. 
The  majority  of  cases  of  aneurysm  do  not  die  from  rupture  of  the 
aneurysm,  but  from  exhaustion  of  the  heart.  This  is  important  to  remember, 
for  the  treatment  is  often  directed  to  the  aneurysm,  whereas  it  is  the  heart 
that  needs  to  be  looked  after. 


CHAPTER   XXVIII 

Adhesive  Mediastino-Pericarditis 

§  226.     Etiology. 

227.  Symptoms. 

228.  Prognosis.     Treatment. 

§  226.  Etiology — The  adherent  pericardium  secondary  to  rheumatic 
pericarditis  rarely  gives  rise  to  any  sign.  In  these  cases  the  pericardium 
is  not  adherent  to  structures  outside  the  heart.  On  the  other  hand, 
certain  obscure  inflammatory  affections,  probably  of  a  tubercular  nature, 
such  as  occur  in  '  polyserositis  ',  give  rise  to  very  marked  phenomena. 
There  is  an  extension  of  an  inflammatory  process  which  affects  all  the  struc- 
tures in  the  mediastinum,  welding  together  the  heart  and  pericardium,  and 
firmly  binding  these  to  all  the  surrounding  structures.  The  heart  becomes 
anchored  to  the  spinal  column  behind  and  to  the  chest-wall  in  front.  As  the 
spinal  column  is  unyielding,  the  contracting  heart  puUs  on  the  ribs  in  front, 
and  as  they  yield  to  a  greater  or  less  extent  we  find  the  ribs  drawn  in  during 
systole  and  springing  back  during  diastole.  This  embarrassment  of  the 
heart  leads  to  great  enlargement  in  its  size,  and  some  of  the  biggest  hearts 
met  with  are  due  to  this  disease. 

§  227.  Symptoms. — The  patients  are  always  very  short  of  breath,  and 
usually  have  to  be  propped  up  when  in  bed.  As  a  rule,  little  or  no  pain  is 
complained  of,  but  in  one  case  I  found  that  attacks  of  angina  pectoris  of 
the  most  severe  form  were  easily  provoked.  A  slight  effort  would  bring 
on  an  attack,  especially  if  the  patient  laughed.  Attacks  could  sometimes 
be  induced  by  pinching  the  skin  under  the  left  nipple,  or  by  applying  the 
stethoscope. 

The  adhesion  of  the  heart  to  the  lungs,  blood-vessels,  and  other  surround- 
ing structures  produces  a  great  variety  of  symptoms,  the  cause  of  many  of 
which  is  obscure.  The  chief  symptoms  are  great  enlargement  of  the  heart — 
so  great  sometimes  as  to  cause  a  marked  difference  between  the  two  sides 
of  the  chest — and  retraction  of  the  structures  surrounding  the  heart  during 
ventricular  systole.  The  systolic  retraction  alone  is  not  distinctive,  as 
I  have  shown  that  it  occurs  when  the  anterior  surface  of  the  heart  is  made 


254 


DISEASES  OF  THE  HEART 


up  of  the  right  ventricle  (Fig.  33).  During  the  ventricular  systole  there  is 
often  an  indrawing  of  the  lower  intercostal  space  on  the  left  side  behind 
(Broadbent's  sign,  Fig.  150).  Tallant  and  Cooper  have  shown  that  this 
may  arise  in  enlargement  of  the  heart  (with  compression  of  the  lungs)  without 
pericardial  adhesion.  In  such  cases,  however,  the  interspaces  affected 
vary  with  respiration,  and  Cooper  suggests  that  when  they  do  not  vary 


Fig.  150.  The  upper  tracing  was  taken  from  the  9th  left 
intercostal  space  behind  from  a  case  of  adhesive  mediastinitis,  and 
shows  '  Broadbent's  sign  ',  which  is  seen  to  be  an  indrawing  of  the 
intercostal  space  during  ventricular  systole  (space  E). 

with  respiration  the  sign  is,  as  Broadbent  states,  an  evidence  of  pericardial 
adhesion.  When  the  chest-wall  is  thin  and  the  heart  is  not  covered  by  lung, 
the  systolic  retraction  of  the  different  interspaces  can  be  seen  in  a  peculiar 
wave-like  rhythm. 

Though  various  murmurs  and  modified  sounds  are  often  heard,  no 
distinctive  sign  can  be  found  on  auscultation.  The  veins  of  the  neck  may 
sometimes  be  seen  to  swell  up  during  inspiration.    A  very  curious  symptom 


Fig.  151.    Simultaneous  tracings  of  the  radial  and  jugular  pulses,  showing  a  great  depression 
(z)  occurring  during  the  ventricular  diastole.     (From  a  case  of  adhesive  mediastinitis.) 

is  a  sudden  collapse  of  these  veins  at  the  beginning  of  diastole,  which 
Friedreich  has  explained  as  due  to  the  springing  back  of  the  ribs  after  the 
ventricular  systole  has  dragged  them  down,  the  cavity  of  the  thorax  being 
thus  suddenly  enlarged  and  expediting  the  flow  from  the  overfilled  veins. 
This  is  well  seen  in  the  jugular  tracing.  Fig.  151,  where  the  fall  z  is  due  to 
the  diastolic  expansion  of  the  chest. 

The  radial  pulse  may  show  a  diminution  in  size  during  inspiration — the 
pulsus  paradoxus.    It  is  now  recognized  that  a  respiratory  variation  of  the 


ADHESIVE  MEDIASTINO-PERICARDITIS  255 

pulse  may  occur  in  a  great  variety  of  conditions,  but  I  think  that  in  adhesive 
mediastinitis  presents  certain  distinctive  features.  Curiously  enough,  no 
tracings  have  been  given,  so  far  as  I  know,  showing  the  pulsus  paradoxus 
in  adhesive  mediastinitis  along  with  the  respiratory  curve,  except  in  two 
instances  taken  by  Nicholson  from  Gibson's  ^^^  cases.  The  study  of  these 
tracings,  compared  with  some  I  have  taken,  leads  me  to  think  that  the 
variations  point  to  very  different  causes.  As,  however,  my  observations 
are  few  in  number,  I  do  not  enter  into  the  subject,  but  call  attention  to 
a  field  that  needs  exploring. 

There  is  usually  associated  with  these  signs  enlargement  and  sometimes 
pulsation  of  the  liver,  which  in  Wenckebach's  *^'  case  was  of  the  auricular 
type.  The  spleen  also  may  be  greatly  enlarged,  and  there  may  be  con- 
siderable dropsy. 

§  228.  Prognosis. — The  future  of  these  cases  is  bad,  though  they 
sometimes  show  periods  during  which  they  make  remarkable  progress 
towards  recovery  from  serious  symptoms.  But  these  are  only  temporary, 
and  they  gradually  drift  to  a  fatal  issue. 

Treatment. — The  treatment  of  these  cases  has  so  far  been  unsatisfac- 
tory, and  one  can  only  advise  the  principles  usual  in  extreme  heart  failure. 
Attempts  have  been  made,  following  the  suggestion  of  Brauer,  to  free  the 
heart  by  resecting  the  ribs.  This  has  been  done  in  several  cases,  and 
Wenckebach*'^'  describes  marked  improvement  in  a  case  in  which  the 
operation  was  performed. 


CHAPTER    XXIX 

Congenital  Affections  of  the  Heart 

§  229.  Etiology. 

230.  Symptoms. 

231.  Prognosis. 

232.  Treatment. 

§  229.  Etiology — Congenital  heart  affections  are  due  to  the  persistence 
of  certain  foetal  forms  of  the  circulation,  such  as  persistent  patency  of  the 
foramen  ovale  or  ductus  arteriosus,  or  to  some  interference  with  development 
leading  to  deformation  of  the  valves  or  narrowing  and  obliteration  of  the 
large  arterial  trunks.  They  may  also  arise  in  consequence  of  foetal  endo- 
carditis.    The  conditions  are  incompatible  with  life  in  many  cases. 

It  is  only  in  exceptional  instances  that  the  symptoms  permit  of  a  recogni- 
tion of  the  nature  of  the  cardiac  defect. 

§  230.  Symptoms. — The  most  characteristic  symptom  is  cyanosis, 
which  is  present  in  a  great  number  of  patients.  Clubbing  of  the  fingers 
is  a  common  accompaniment  of  the  cyanosis.  The  size  of  the  heart  is  often 
greatly  increased.  This  may  be  due  to  hypertrophy  of  the  left  ventricle 
when  there  is  an  obstruction  to  the  outflow  of  the  blood  through  the  aorta, 
or  to  dilatation  of  the  right  heart  when  there  is  interference  with  the  pul- 
monary circulation  or  a  patent  foramen  ovale.  Murmurs  are  usually  present, 
almost  invariably  systolic  in  time,  but  it  is  difficult  to  detect  their  origin 
except  in  the  case  of  the  patent  ductus.  Here  the  communication  between 
the  aorta  and  pulmonary  artery  persists,  and  as  the  pressure  is  much  higher 
in  the  aorta  a  continuous  stream  passes  during  the  whole  cardiac  cycle 
from  the  aorta  to  the  pulmonary  artery,  and,  as  Gibson ^^'  has  pointed  out, 
this  leads  to  a  murmur  which,  beginning  with  great  intensity  at  ventri- 
cular systole,  extends  over  ventricular  systole  into  diastole,  fading  away 
towards  the  end  of  diastole.  This  murmur  is  loudest  over  the  second  and 
third  left  interspaces,  and  here  also  a  well-marked  thrill  synchronous  with 
the  murmur  can  be  felt. 


CONGENITAL  AFFECTIONS  OF  THE  HEART  257 

§  231.  Prognosis — If  there  be  no  cyanosis,  little  or  no  enlargement  of 
the  heart,  and  the  development  of  the  child  good,  with  a  fair  field  of  cardiac 
response,  then  the  prognosis  is  good  ;  otherwise  the  outlook  is  bad,  though 
the  child  may  lead  a  crippled  existence  for  many  years. 

§  232.  Treatment — If  the  heart  maintains  the  circulation  well,  no 
treatment  is  required.  In  more  serious  cases,  beyond  attending  to  the 
child's  comfort  and  nourishment,  special  treatment  for  the  heart  is  of  little 
benefit,  digitalis  being  rarely  of  value  unless  there  is  dropsy. 


MACKENZIE 


CHAPTER   XXX 

Heart  Disease  and  Pregnancy 

§  233.     Importance  of  the  subject. 

234.  Standards  for  guidance. 

235.  Management  of  the  labour. 

§  233.  Importance  of  the  subject. — It  is  almost  certain  to  be  the 
experience  of  every  practitioner  who  has  a  midwifery  practice  to  be  met 
by  the  question  of  pregnancy  in  women  with  some  affection  of  the  heart, 
and  this  question  is  of  supreme  importance,  for  life  and  death  depend  upon 
the  views  held  by  the  doctor.  If  the  gravity  of  the  question  is  not  sufficiently 
appreciated,  the  consequences  in  certain  cases  may  be  ruined  health  or  even 
the  death  of  the  woman,  while  a  too  serious  view  of  other  cases  may  unjustly 
entail  upon  the  woman  an  uncalled-for  restraint.  Hitherto  the  guide  in 
the  diagnosis  has  been  in  the  main  the  presence  of  a  valvular  murmur,  and 
some  doctors,  having  seen  patients  with  valvular  lesions  pass  scatheless 
through  repeated  pregnancies,  treat  the  subject  too  lightly,  while  others, 
who  have  witnessed  the  disastrous  results  of  pregnancy,  are  oppressed  by 
the  gravity  of  the  condition. 

The  treatise  on  The  Bearings  of  Chronic  Diseases  of  the  Heart  upon 
Pregnancy,  Parturition,  and  Childbed,  by  Angus  Macdonald,  in  1878,  is  stiU 
the  best  work  on  the  subject,  and  long  experience  and  observation  lead  me 
to  agree  with  him  in  most  points.  The  researches  on  this  subject  have  too 
often  been  directed  to  the  somewhat  barren  and  academic  question  as  to 
whether  the  heart  hypertrophies  during  pregnancy,  and  the  bearing  of  this 
on  prognosis.  If,  however,  it  be  borne  in  mind  that  heart  failure  is  essentially 
a  question  of  the  integrity  of  the  heart  muscle,  a  better  standpoint  will  be 
obtained  for  judging  these  cases.  The  valve  lesion  in  the  great  majority 
is  at  the  most  only  an  embarrassment  to  the  heart  in  its  work,  and  one 
which  it  may  easily  overcome.  The  presence  of  the  lesion  is  important, 
however,  in  another  respect,  namely,  in  that  it  calls  attention  to  the  heart 
and  serves  to  remind  us  that  the  disease  that  injured  the  valve  may  at  the 
same  time  "have  injured  the  muscle  :  our  object  in  examining  these  cases 
is  to  find  out  the  extent  of  the  lesion  in  the  muscle,  and  how  far  the  valve 
lesion  embarrasses  the  muscle. 


HEART  DISEASE  AND  PREGNANCY  259 

§  234.  Standards  for  guidance — The  essential  question  in  cases  of 
valve  disease  is  the  condition  of  the  muscle,  and  this  is  determined  by  the 
manner  in  which  the  heart  responds  to  effort.  Additional  help  will  be 
obtained  by  noting  the  size  of  the  heart,  its  rate  and  rhythm,  and  the 
tendency  to  oedema  of  the  legs  and  lungs.  Given  a  fair  field  of  cardiac 
response  with  little  or  no  enlargement  of  the  heart,  then  pregnancy  need 
have  no  terrors.  If  the  field  of  cardiac  response  is  distinctly  limited, 
particularly  if  palpitation  is  readily  induced  by  exertion,  with  no  oedema, 
then  the  opinion  should  be  suspended  till  the  result  of  treatment  is  ascer- 
tained. If  the  condition  does  not  improve,  then  the  outlook  is  not  hopeful, 
and  pregnancy  should  be  forbidden. 

With  the  appearance  of  dilatation  and  its  accompanying  symptoms — 
oedema  of  the  legs  and  lungs — pregnancy  should  be  forbidden.  In  doubtful 
cases,  with  some  dilatation  and  no  swelling  of  the  legs,  I  have  been  accus- 
tomed to  be  guided  by  the  tendency  to  oedema  of  the  lungs.  This  is  readily 
ascertained  by  examining  the  patient  after  a  night's  rest,  before  she  gets  up. 
If  she  be  instructed  to  lie  on  one  side  as  much  as  possible,  and  not  to  sit  up 
until  she  is  examined,  numerous  fine  crepitations  will  be  found  on  the  first 
deep  inspiration,  if  there  be  any  tendency  to  oedema.  The  auscultation 
of  the  lung  base  should  be  the  first  procedure  adopted  in  the  examination. 
If  the  crepitations  are  dispelled  with  the  first  few  deep  inspirations,  then  it 
may  be  taken  for  granted  that  there  is  only  a  slight  tendency  to  oedema, 
and  the  case  requires  care  and  watchfulness  before  finally  deciding.  If  the 
crepitations  persist,  then  the  tendency  to  oedema  is  so  great  that  pregnancy 
should  be  forbidden  (see  also  §  190). 

It  must  be  kept  in  mind  that  patients  with  valvular  lesion  may  suffer 
from  most  severe  heart  failure  (dilatation,  and  extensive  dropsy),  and  make 
such  good  recoveries  that  repeated  pregnancies  may  be  undertaken  with 
impunity.  Here,  however,  the  degree  of  recovery  gives  the  standard  for  the 
judgment,  and  I  mention  this  lest  the  knowledge  of  a  bygone  heart  failure 
be  considered  a  bar  to  marriage  and  pregnancy. 

One  of  the  most  difficult  problems  I  have  had  to  face  has  been  where 
a  pregnant  woman  has  shown  evidence  of  heart  failure,  and  the  question 
has  arisen  whether  interference  is  necessary.  For  one  thing,  a  natural 
labour  entails  less  strain  upon  the  heart  than  one  artificially  induced.  In 
the  former  case  the  preliminary  preparation  and  softening  of  the  tissue 
render  the  expulsion  of  the  child  much  easier,  even  though  the  head  is  larger. 
But,  on  the  other  hand,  the  dropsy  may  increase  to  such  an  extreme  degree 
that  no  aid  can  be  rendered. 

One  of  my  most  painful  experiences  was  in  the  case  of  a  woman  of 

s  2 


260  DISEASES  OF  THE  HEART 

thirty-five  years  of  age  with  mitral  stenosis,  who  became  pregnant  with  her 
first  child ;  when  labour  set  in  the  dropsy  had  become  so  extensive,  and  the 
breathlessness  so  great,  that  she  could  not  lie  down,  but  had  to  sit  up  in  bed. 
It  was  impossible  to  make  a  vaginal  examination,  as  she  could  not  turn  to 
one  side  without  great  suffering.  She  could  not  take  chloroform,  as  the 
inhalation  intensified  the  dyspnoea,  and  we  were  helpless,  and  had  to  see 
her  die  after  thirty-six  hours  of  suffering,  relieved  slightly  by  opium.  In 
other  cases  where  the  dropsy  and  breathlessness  were  threatening  to  become 
extreme,  I  have  successfully  induced  premature  labour.  Fortunately, 
many  women  with  advanced  heart  failure  abort.  Ii  others  abundant 
bleeding  from  a  varicose  vein  gives  great  relief,  and  suggests  venesection 
when  there  is  much  evidence  of  over-filling  of  the  venous  system. 

The  nodal  rhythm  should  be  a  bar  to  pregnancy  in  aU  cases. 

Although  the  valvular  lesion  by  itself  is  not  a  contra-indication,  yet  the 
particular  valvular  lesion  influences  the  decision  when  it  is  combined  with 
indications  of  muscle  failure.  Thus  aortic  lesions  are  very  serious  unless 
there  be  a  good  intact  heart  muscle.  Mitral  stenosis,  when  there  is  only 
a  presystolic  murmur  and  good  effective  muscle,  is  no  bar  ;  but  if  there  is 
also  a  diastolic  murmur,  then,  unless  the  muscle  is  very  good,  pregnancy 
should  not  be  permitted,  as  the  diastolic  murmur  points  to  a  progressive 
narrowing  of  the  orifice. 

§  235.  Management  of  the  labour — In  regard  to  the  management 
of  labour  in  these  patients  with  heart  affections,  if  there  is  the  slightest 
sign  of  heart  failure  the  patient  should  be  instructed  not  to  bear  down, 
and  chloroform  should  be  administered  very  early,  the  anaesthesia  being 
gradually  deepened.  As  soon  as  it  is  feasible,  forceps  should  be  appHed, 
and  gentle,  firm  traction  intermittently  maintained  until  delivery  is  effected 
— even  if  the  forceps  have  to  be  on  for  a  considerable  time. 

I  have  never  seen  the  slightest  risk  from  chloroform  in  these  cases. 

After  the  delivery  is  over  the  patient  is  not  out  of  danger,  for  symptoms 
of  severe  heart  failure  may  supervene  any  time  within  the  next  three  weeks. 
In  view  of  this,  care  should^be  taken  to  ease  the  heart's  work,  by  rendering 
the  patient  comfortable  and  inducing  refreshing  sleep.  In  severe  cases 
nursing  the  child  is  out  of  the  question,  nor  should  the  child  be  allowed  to 
disturb  the  mother.  The  judicious  administration  of  digitalis  is  of  service, 
following  the  lines  laid  down  in  Chapter  XXXIV. 


CHAPTER  XXXI 

Chloroform  in  Heart  Affections 

§  236.     Conditions  contra-indicating  its  use :    respiratory  embarrassment,   cardio-sclerosis, 
status  lymphaticus. 
237.     Estimation  of  the  fitness  of  the  patient. 

§  236.  Conditions  contra-indicating  its  use — For  a  number  of  years 
I  made  numerous  careful  observations  on  patients  to  see  if  I  could  detect 
any  special  action  of  chloroform  on  the  heart.  I  got  various  alterations 
in  the  pulse-rate,  and  in  the  degree  of  venous  engorgement,  but  these 
were  in  the  main  due  to  the  patient  being  excited  or  struggling,  or  holding 
his  breath,  so  that  I  could  detect  no  sign  of  any  direct  influence  of  the 
chloroform  on  the  heart.  It  must  be  borne  in  mind  that  a  great  many  of 
the  physiological  experiments  have  been  carried  out  with  very  large  doses, 
and  with  the  animal's  heart  in  a  very  unnatural  condition,  so  that  the  results 
cannot  be  compared  with  those  of  the  small  doses  given  to  a  human  being. 

The  question  whether  a  patient  can  take  chloroform  has  often  to  be 
met,  and  the  indications  against  its  administration  have  never  been  clearly 
given.  The  stethoscopic  examination  of  the  patient  just  before  administra- 
tion is  useless  ;  the  decision  must  be  made  independently  of  any  results 
obtained  by  it,  for  no  form  of  murmur,  irregularity,  or  rate  is  a  bar  to  the 
administration  of  chloroform.  I  am  not  aware  of  a  single  form  of  heart 
ailment  discoverable  by  auscultation  that  would  render  the  administration 
of  chloroform  dangerous.  The  dangers  do  not  lie  in  the  action  of  chloroform 
upon  the  heart  alone,  but  on  other  considerations.  Thus,  there  is  often 
trouble  and  even  danger  in  giving  chloroform  to  emphysematous  people 
with  great  liability  to  bronchitis,  and  to  elderly  people  with  a  tendency  to 
bronchitis  and  with  wheezing  rales  accompanying  respiration,  and  also  in 
cases  of  embarrassment  of  the  lungs  from  oedema,  abundant  pleural 
effusion,  or  tumours  pressing  on  the  windpipe — in  fact,  all  cases  with 
imperfect  oxygenation  of  the  blood. 

Elderly  people  with  a  suspicion  of  cardio-sclerosis  are  also  bad  subjects, 
not  because  of  the  chloroform,  but  because  their  hearts  are  unable  to  with- 
stand even  sHght  strains.  Thus  one  typical  cardio-sclerotic  who  was  to 
be  operated  upon  for  piles,  and  who  had  suffered  from  intense  irritation 
about  the  anus,  and  was  most  anxious  to  be  relieved,  had  shown  signs 


262  DISEASES  OF  THE  HEART 

of  slight  attacks  of  angina  pectoris.  He  was  greatly  excited  on  entering 
the  operating  room,  and  when  laid  down  preparatory  to  receiving  the  chloro- 
form his  pulse  was  very  rapid.  The  towel  had  just  been  placed  over  his 
face  when  his  pulse  stopped.  The  towel  was  at  once  removed,  and  he  con- 
tinued to  respu-e  with  considerable  force  for  a  few  minutes  and  then  stopped, 
and  he  was  dead.  Manifestly  it  was  not  the  chloroform  that  killed,  but  the 
strain  on  the  enfeebled  heart. 

The  Status  Lymphaticus. — Of  late  years,  a  number  of  deaths  have 
occurred  in  a  condition  described  as  the  status  lymphaticus.  I  have  no 
experience  of  this  condition  myself,  but  it  is  described  as  a  state  in  which 
the  sufferer  may  die  from  any  trivial  cause,  and  which  is  marked  by  enlarged 
thymus  and  spleen,  hypertrophied  lymphatic  glands  in  various  regions, 
with  swelling  of  the  tonsils,  and  of  the  solitary  follicles  and  Peyer's  patches 
in  the  intestine,  and  flaccid  cardiac  muscle.  The  condition  may  be  recognized 
during  life  from  the  pale  thin  skin  and  pasty  complexion  and  fairly  abundant 
subcutaneous  fat,  along  with  frequent  signs  of  rickets  or  scrofula,  enlarge- 
ment of  the  tonsils  and  of  the  superficial  glands,  especially  in  the  axilla 
and  neck,  adenoid  growths,  a  palpable  spleen,  and  often  enlargement  of 
the  thyroid  (McCardie). 

§  237.  Estimation  of  the  fitness  of  the  patient — It  will  be  seen  that 
the  examination  of  the  patient  should  be  made  prior  to  his  reaching  the 
table,  and  if  there  is  a  doubt,  even  a  day  or  two  before  the  operation. 
Apart  from  the  status  lymphaticus,  the  best  test  is  the  patient's  field  of 
cardiac  response.  But  even  when  the  field  is  greatly  limited  from  some 
exhausting  disease,  with  or  without  valvular  affection,  the  patient  may  take 
chloroform  with  safety.  In  these  circumstances,  the  operation  is  sometimes 
delayed  for  days  or  weeks  in  order  that  the  heart  may  be  strengthened  by 
drugs  like  strychnine  and  digitalis.  Now  this  is  very  bad  practice,  for  it 
may  be  taken  for  granted  that  no  patient's  heart  will  gain  strength  while 
an  operation  is  hanging  over  his  head,  more  particularly  if  he  or  she  knows 
that  the  operation  is  delayed  for  the  heart  to  be  strengthened.  I  can 
conceive  of  nothing  better  calculated  to  weaken  the  heart  than  such 
a  procedure,  for  the  anxiety  is  bound  to  react  upon  the  heart  and  make 
it  more  irritable.  When  a  patient  with  a  weak  heart  is  to  be  operated  on, 
the  sooner  it  is  done  the  better. 

Under  the  influence  of  excitement  and  fear,  the  patient's  heart  may 
appear  worse  than  it  is,  and  one  should  always  keep  that  in  mind  when  the 
heart  is  behaving  strangely  before  an  operation,  as  the  following  illustration 
shows.  I  proposed  to  remove  a  large  ovarian  cyst  from  a  very  intelligent 
patient  ;    all  arrangements  were  made,  and  when  I  arrived  in  the  morning 


CHLOROFORM  IN  HEART  AFFECTIONS  263 

to  do  the  operation  I  was  informed  that  the  patient  had  gone  out  of  her 
mind,  and  that  her  heart  was  very  bad.  When  I  saw  her  she  was  muttering 
incessantly,  and  took  no  notice  of  any  question  I  put  to  her.  Her  pulse 
was  extremely  small  and  very  rapid,  160  beats  per  minute.  After  reflecting 
over  the  case  I  concluded  that  the  condition  was  in  all  likelihood  due  to 
apprehensive  fear,  and  that  chloroform  would  be  likely  to  soothe  the  brain 
and  relieve  the  heart,  so  that  to  delay  the  operation  would  but  add  to  the 
terror  of  the  patient  when  she  recovered.  I  therefore  asked  the  anaesthetist 
to  proceed,  but  he  refused,  and  I  started  the  chloroform  myself.  She  went 
under  very  quickly,  and  the  pulse  speedily  fell  to  seventy  beats  per  minute, 
at  which  rate  it  remained  during  the  operation,  and  when  she  came  out  of 
the  chloroform  she  was  perfectly  rational,  and  made  a  good  recovery. 

I  have  administered  chloroform  repeatedly  in  cases  of  extreme  heart 
failure  with  valvular  lesions — for  example,  during  labour,  and  in  one  case 
where  the  patient  appeared  to  be  dying  from  a  severe  attack  of  pneumonia — 
and  I  have  never  seen  the  slightest  bad  effect  from  the  chloroform.  Cases 
with  extreme  irregularity  of  the  heart  can  take  chloroform  without  danger. 
I  watched  for  a  whole  hour  a  case  of  complete  heart-block  under  full 
anaesthesia. 

The  cause  of  death  under  chloroform  anaesthesia — apart  from  over- 
dose and  imperfect  aeration  of  the  blood — has  so  far  escaped  recognitiqn. 
It  is  probable  that  the  secret  lies  in  the  fact  that  certain  changes,  as  yet 
unknown,  render  some  hearts  abnormally  susceptible  to  the  action  of 
chloroform.  One  can  infer  this  from  the  effect  of  digitalis,  which  is  shown 
in  Chapter  XXXIV  to  have  a  varied  action  depending  on  the  nature  of  the 
heart  lesion.  At  all  events,  no  satisfactory  conclusion  will  ever  be  reached 
until  graphic  records  of  the  movements  of  the  circulation  and  respiration 
are  made  during  the  whole  time  of  anaesthesia.  As  death  occurs  quite 
unexpectedly,  it  would  be  necessary  to  make  observations  consecutively 
on  many  thousands  of  cases. 


CHAPTER   XXXII 
Prognosis 

§  238.    Responsibility  of  the  medical  profession. 
239.    Basis  for  prognosis. 

§  238.  Responsibility  of  the  medical   profession In  addition  to 

recognizing  the  meaning  of  any  abnormal  sign  or  symptom,  we  should 
endeavour  to  acquire  a  knowledge  of  what  bearing  it  has  upon  the  future 
history  of  the  patient.  This  knowledge  can  only  be  obtained  by  watching 
how  patients  exhibiting  the  abnormality  meet  the  storm  and  stress  of  life. 
This  has  been  a  special  object  of  my  work  on  the  heart  for  over  a  quarter 
of  a  century,  and  in  the  following  observations  I  am  culling  from  my  own 
personal  experience,  and  in  each  deduction  I  give  I  have  in  my  mind 
a  number  of  cases  from  which  it  has  been  drawn. 

I  am  rather  afraid  that  our  profession  as  a  body  does  not  recognize 
sufficiently  its  responsibility  in  regard  to  prognosis.  When  an  individual 
submits  himself  for  an  opinion,  he  does  so  with  such  implicit  confidence 
that  the  verdict  given  may  alter  the  whole  tenor  of  his  life.  He  may  be, 
for  instance,  seeking  to  enter  some  profession,  when  a  preliminary  medical 
examination  reveals  what  the  medical  man  takes  to  be  an  abnormality. 
An  imperfect  knowledge  of  its  nature  may,  and  unfortunately  often  does, 
lead  to  its  being  regarded  as  presaging  possibly  grave  consequences,  and  the 
candidate  is  rejected.  He  is  thus  shut  off  from  the  prospect  of  his  chosen 
calling,  and,  knowing  the  reason  of  his  rejection,  passes  through  life  uneasily 
conscious  that  some  disaster  is  always  impending,  while  aU  the  time  the 
supposed  abnormality  may  be  a  sign  of  little  or  no  consequence. 

If  we  look  at  an  insurance  paper  we  realize  the  hardships  to  which  an 
applicant  is  exposed.  Is  the  pulse  regular  ?  Are  the  sounds  pure  ?  If 
either  question  is  answered  in  the  negative,  the  applicant  is  either  rejected 
or  is  penalized  for  life  by  having  to  pay  a  higher  premium,  and,  in  addition, 
is  burdened  with  the  painful  consciousness  of  infirmity. 

I  dwell  on  this  matter  with  some  insistence,  because  I  have  known  of 
so  many  instances  in  which  gross  injustice  has  been  done  to  individuals, 
not  only  in  the  pecuniary  aspect,  but  in  having  imposed  upon  them  great 
expense,  unnecessary  treatment,  and  mental  disquiet,  because  the  meaning 


PROGNOSIS  265 

and  prognostic  significance  of  some  simple  symptom,  as  a  murmur  or  an 
extra-systole,  have  not  hitherto  been  recognized.  I  sometimes  wonder 
whether  the  use  of  auscultation  has  not  been  the  means  of  doing  more  harm 
than  good.  That  it  is  not  an  unalloyed  blessing  is  too  painfully  evident, 
for  not  only  have  totally  incorrect  conclusions  been  drawn  as  to  the  bearing 
of  murmurs  on  the  future  of  the  patient,  but  so  much  time  has  been  spent 
in  investigating  the  physics  of  their  production  that  more  important  matters 
have  been  lost  sight  of.  It  is  so  easy  to  recognize  a  murmur,  that  other  less 
obvious  but  more  significant  signs  have  too  often  been  neglected. 

A  serious  responsibility  is  thrown  upon  every  practitioner  at  times  in 
advising  upon  other  questions.  Should  a  man  give  up  his  business  ?  is  a 
question  on  which  advice  is  constantly  sought,  and  whether  the  individual  be 
a  statesman  or  a  labourer  the  greatest  care  is  necessary  in  formulating  the 
answer.  Should  a  woman  with  some  heart  affection  marry,  or,  if  she  is 
pregnant,  should  the  pregnancy  be  allowed  to  proceed  ?  are  problems  that 
every  general  practitioner  at  one  time  or  another  will  have  to  meet  ;  and 
if  he  seeks  for  guidance  in  the  textbooks  he  finds  merely  general  views 
which  he  cannot  apply  to  the  individual  case.  This  fact  alone  should  arrest 
the  attention  of  the  profession,  and  make  it  conscious  how  inefficient  the 
teaching  of  heart  affections  has  been. 

§  239.  Basis  for  prognosis — A  rational  prognosis  must  be  based  on 
a  clear  idea  of  the  manner  in  which  any  given  symptom  is  produced. 
Knowledge  never  dispelled  the  terrors  of  darkness  with  more  effect  than  in 
showing  the  true  meaning  of  the  symptoms  in  affections  of  the  heart.  So 
impressed  are  the  public  and  profession  with  the  suddenness  with  which 
death  may  take  place,  that  an  unnecessary  fear  lays  hold  of  them  when  the 
heart  shows  any  sign  out  of  the  common,  lest  this  should  be  the  thing  that 
slays.  It  is  because  of  this  that  I  have  entered  with  such  fuUness  into  the 
explanation  of  so  many  symptoms.  I  confess  there  are  still  many  which 
I  do  not  understand,  but  I  have  endeavoured  to  find  out  their  value  by 
watching  individuals  who  exhibited  them,  and  to  find  a  basis  on  which  their 
value  can  be  estimated. 

In  estimating  the  value  of  any  abnormal  sign,  or  in  determining  the 
condition  of  a  heart,  the  most  reliable  guide  is  the  manner  in  which  the  heart 
responds  to  exertion.  This,  again,  is  but  an  attempt  to  estimate  the  amount 
of  reserve  force.  If  the  individual  can  with  comfort  make  such  exertions  as 
we  would  expect  at  his  time  of  life,  then  the  abnormaUty  may  with  certainty 
be  assumed  to  be  of  little  real  significance. 

If  there  be  a  complete  breakdown,  the  decision  should  not  be  made  until 
time  has  shown  to  what  extent  recovery  takes  place.       The  amount  of 


266  DISEASES  OF  THE  HEART 

recovery  enables  us  to  judge  the  condition  of  the  muscle  of  the  heart,  for 
it  is  on  its  capability  to  renew  its  reserve  force  that  the  future  of  the  patient 
depends.  To  illustrate  this  I  cite  the  history  of  a  man  whose  case  is  also 
described  in  the  Appendix  for  other  reasons  (Case  17,  Appendix  IV). 

In  1883,  at  the  age  of  thirty-two,  the  patient  had  a  severe  attack  of 
rheumatic  fever,  and  was  left  with  a  mitral  lesion.  In  1897  he  lay  for  weeks 
unconscious  and  swollen  with  dropsy.  From  this  he  recovered  with  a  well- 
marked  presystolic  and  diastolic  mitral  murmur  and  a  slightly  enlarged  heart. 
In  1904  his  heart  became  continuously  irregular,  and  has  remained  so  ever 
since.  It  now  extends  two  inches  beyond  the  nipple  line,  and  he  has  a 
systolic  and  long  diastolic  mitral  murmur.  Notwithstanding  all  this,  for  the 
past  four  years  he  has  followed  his  trade  as  a  mechanical  engineer,  doing 
the  very  hardest  work  of  this  laborious  trade,  and  from  1904  to  1906  he 
worked  overtime  almost  daily.  Beyond  being  somewhat  short-winded 
going  uphill,  especially  in  cold  weather,  he  feels  as  fit  for  work  as  ever 
he  did. 

Even  cases  that  never  show  so  complete  restoration  of  function  as  this, 
and  in  which  attacks  of  extreme  failure  are  frequent,  may  go  on  for  many 
years  and  lead  sometimes  fairly  useful  lives,  though  in  time  the  progressive 
changes  become  so  great,  or  the  muscle  so  exhausted,  that  the  possibility  of 
even  temporary  recovery  is  precluded. 

In  individuals  in  whom  there  is  a  distinct  limitation  of  the  field  of  cardiac 
response,  a  close  scrutiny  should  be  made  into  the  cause.  It  should  be 
borne  in  mind  that  if  a  heart  is  not  properly  exercised  its  field  of  response 
becomes  more  and  more  restricted.  Thus  a  man  who  for  a  long  time  leads 
a  sedentary  life  is  often  startled  by  the  fact  that  he  is  rendered  extremely 
breathless  by  undertaking  some  exertion  that  he  was  wont  to  make  with 
ease  a  few  years  previously.  But  with  moderate  training  there  is  soon 
restored  sufficient  reserve  force  to  enable  him  to  perform  his  task  without 
distress.  Therefore  in  all  cases,  even  when  there  is  an  abnormal  symptom — 
as  a  murmur  or  an  irregularity — this  question  of  the  nature  of  the  exhaustion 
should  be  borne  in  mind.  It  must  not  be  forgotten  also  that  the  supposed 
abnormaUty  may  have  nothing  to  do  with  the  symptoms  of  exhaustion. 
This  is  particularly  the  case  in  the  young,  in  whom  syncopal  attacks  are 
not  infrequent.  I  have  repeatedly  seen  grave  alarm  aroused  because  a  boy 
or  girl  has  fainted,  and  has  had  an  irregular  pulse  when  quiet  in  bed.  This 
irregularity  has  been  of  the  youthful  type  (sinus  irregularity),  and  if  it  had 
any  connexion  with  the  syncopal  attacks  it  was  merely  incidental,  and  in 
no  sense  added  any  gravity  to  a  trivial  affection. 

While  the  lines  on  which  prognosis  is  based  can  be  fairly  well  recognized 


PROGNOSIS  267 

in  regard  to  the  more  common  affections  of  the  heart,  we  often  meet  with 
patients  who  show  symptoms  whose  nature  is  too  obscure  for  us  to  identify. 
A  prognosis  in  these  cases  is  often  required  and  difficult  to  give.  The  plan 
I  have  adopted  is  to  exclude  the  possibility  of  degenerated  muscle  by  an 
analysis  of  the  condition  of  the  separate  functions  of  the  heart  muscle, 
and  consider  how  far  the  complaints  may  be  nervous  in  origin  ;  having 
satisfied  myself  that  the  muscle  is  sound,  I  give  a  favourable  prognosis, 
at  the  same  time  indicating  the  obscurity  of  the  case.  I  do  this  because, 
as  a  matter  of  experience,  I  have  found  that  these  exceptional  cases,  particu- 
larly in  young  adults,  always  tend  to  recovery  to  a  greater  or  less  degree. 
This  unfortunately  is  not  the  usual  plan,  for  some  signs  are  too  often 
taken  to  be  more  serious  the  more  obscure  they  are.  In  many  cases  the 
physician  must  be  prepared  to  back  up  his  opinion  by  taking  a  grave  amount 
of  responsibility.  For  instance,  I  have  on  several  occasions  seen  patients 
kept  in  bed  and  put  through  elaborate  forms  of  treatment  after  some  such 
affection  as  influenza.  The  patients  have  complained  of  obscure  signs,  to 
them  alarming,  and  a  certain  amount  of  abnormality  has  been  present,  as 
frequent  pulse  or  extra-systoles.  Having  satisfied  myself  that  there  was  no 
serious  mischief,  I  have  had  no  hesitation  in  making  the  patients  get  up  and 
resume  their  ordinary  life,  even  when  the  medical  attendant  has  shrunk 
from  the  responsibility.  I  have  never  yet  had  cause  to  regret  such  a  pro- 
cedure, and  it  is  better  to  run  a  little  risk  in  a  rare  case  than  to  have  a 
patient  drifting  on  to  invalidism  because  of  our  ignorance  and  fear  of 
responsibility. 


CHAPTER   XXXIII 

Treatment 

§  240.  Tlie  essential  principle  in  treatment. 

241.  Rest. 

242.  Sleep. 

243.  Bodily  comfort. 

244.  Diet. 

245.  Condition  of  the  bowels. 

246.  The  mental  factor. 

247.  Drugs. 

248.  Oxygen. 

§  240.    The  essential  principle   in    treatment In   order   to  treat 

failure  of  the  heart  intelligently  it  is  necessary  to  find  out  some  principle 
which  will  serve  as  a  guide.  So  far  as  the  heart  is  concerned  we  get  a  safer 
guide  than  is  possible  for  any  other  viscus,  as  the  nature  of  its  failure  can  be 
more  easily  ascertained.  As  in  all  forms  of  heart  affections  exhaustion  of 
the  reserve  force  is  the  essential  factor  in  the  failure,  so  the  restoration  of 
this  reserve  force  is  the  aim  and  object  of  treatment.  But  in  the  first  place 
an  accurate  diagnosis  should  be  made,  and  if  we  detect  some  change  which 
alarms  the  patient,  but  is  really  of  Httle  significance,  as  certain  murmurs  or 
irregularities,  then  the  reassurance  of  the  patient  as  to  the  innocent  nature 
of  his  trouble  brings  relief ;  or  if  we  detect  some  permanent  change  it  is 
useless  to  waste  time  and  energy  in  the  haphazard  prescription  of  supposed 
remedies.  It  is  futile  to  imagine  that  we  can  restore  a  cicatrized  valve, 
a  sclerotic  myocardium,  or  a  calcareous  artery  to  their  pristine  condition. 
We  must  recognize  facts,  and,  with  the  knowledge  of  the  presence  of  such 
irremediable  conditions,  endeavour  to  make  the  best  of  the  heart  muscle 
that  is  left. 

Whatever  may  be  the  nature  of  the  organic  lesion,  the  immediate  heart 
failure  in  any  given  case  is  due  to  the  heart  having  to  undertake  work  which 
makes  a  call  upon  the  reserve  force,  while  the  period  of  rest  is  not  suffi- 
ciently long  to  permit  it  to  recuperate.  Step  by  step  the  exhaustion  pro- 
ceeds till  some  striking  evidence  of  this  heart  failure  finally  compels  the 
patient's  attention.  If  this  conception  of  the  cause  of  the  heart  failure 
be  grasped,  we  are  at  once  placed  in  a  position  to  undertake  a  rational  treat- 


TREATMENT  269 

ment  ;  the  principle  of  such  treatment  is  so  simple  that  it  seems  almost 
unnecessary  to  dwell  upon  it,  namely,  the  placing  of  the  heart  in  a  position 
to  regain  its  reserve  force.  This  principle  is  so  obvious  that  it  is  apt  to  be 
ignored,  but  when  any  successful  form  of  special  treatment  is  investigated, 
it  will  be  found  that  its  success  is  due  to  the  unconscious  adoption  of  this 
principle. 

The  next  step  to  be  taken  after  recognizing  the  principle  is  to  find  out 
what  functions  of  the  heart  muscle  are  exhausted.  This,  as  a  rule,  can 
be  ascertained  by  methodical  inquiry  into  all  the  symptoms  after  the 
manner  I  have  detailed  in  the  text.  The  adoption  of  special  measures 
when  necessary  will  follow  the  result  of  this  examination  into  the  nature 
of  the  failure,  and  these  I  have  indicated  under  the  description  of  the 
different  symptoms.  Here  I  will  dwell  more  on  the  general  appUcation 
of  principles  suitable  to  the  treatment  of  the  great  majority  of  cases  of 
heart  failure. 

§  241.  Rest. — On  examination  we  may  find  evidence  of  some  organic 
change  in  the  heart,  as  a  valvular  murmur,  persistent  irregularity,  or  dilata- 
tion, and  then  we  recognize  that  the  heart  has  not  only  been  doing  the  work 
incumbent  on  a  healthy  heart,  but  it  has  been  doing  so  hampered  byjts 
own  inherent  defect.  As  we  cannot  modify  the  latter  condition  we  must 
seek  to  ease  the  load  in  the  other  direction,  and  it  is  here  that  the  physician 
has  to  exercise  a  very  wise  discretion.  He  should  enter  into  the  patient's 
daily  life  and  find  out  the  circumstances  that  are  likely  to  induce  heart 
exhaustion.  To  give  up  the  work  by  which  the  patient  earns  his  Uvelihood 
may  be  too  serious  a  matter,  but  the  physician  may  be  able  to  suggest  the 
omission  of  certain  kinds  of  work  that  may  relieve  the  strain  without  inter- 
fering too  seriously  with  the  patient's  employment.  Or  it  may  be  that 
some  habit,  as  over-indulgence  in  alcohol  or  tobacco,  or  some  dietetic  error, 
can  be  corrected  with  benefit.  Besides  relieving  the  heart  from  over- 
work, it  must  be  placed  in  a  position  to  do  its  work  as  free  from  irritation 
as  possible.  The  great  influence  which  the  nervous  system  has  on  the  heart 
must  always  be  borne  in  mind.  A  worried  and  anxious  mind  invariably 
reacts  on  the  heart,  rendering  it  unstable  or  excitable.  This  factor  is  of 
such  importance  that  when  the  question  of  work  arises,  if  it  is  found  that 
the  cessation  of  work  results  in  mental  worry  and  disquiet,  it  is  far  safer 
to  allow  the  patient  to  follow  his  occupation  Avith  discretion,  and  with 
due  regard  to  the  nature  of  the  work.  In  severe  heart  failure,  it  is  scarcely 
necessary  to  say,  rest  in  bed  is  imperative. 

§  242.   Sleep — Whatever  the  form  the  heart  failure  may  assume,  sleep 
is  essential.    It  may  be  taken  as  an  axiom  that  if  the  patient  does  not  get 


270  DISEASES  OF  THE  HEART 

sufficient  sleep  he  will  never  get  well.  Inquiries  should  be  made  of  every 
patient  in  regard  to  his  sleep  ;  if  it  is  not  good  and  cannot  be  attained  by 
removing  all  forms  of  bodily  discomfort,  then  resort  must  be  had  to  soporifics. 
If  an  individual  has  been  accustomed  to  some  alcohol — beer,  stout,  or 
whisky — at  bedtime,  and  the  want  of  it  results  in  sleeplessness,  then  he  should 
be  allowed  to  have  it.  The  milder  hjrpnotics  may  be  tried,  as  antifebrin, 
veronal,  or  sulphonal,  but  if  these  fail  resort  must  be  had  to  chloral  and 
opium.  In  great  restlessness  from  breathlessness,  cardiac  asthma,  Cheyne- 
Stokes  respiration,  these  drugs  must  be  carefuUy  pushed  until  the  desired 
effect  has  been  obtained.  As  to  the  selection  of  the  drug,  in  serious  cases 
I  have  found  chloral  the  safer  and  more  useful  when  there  is  little  or  no 
dilatation  of  the  heart,  when  the  blood-pressure  is  high,  as  in  cardio-sclerosis, 
and  when  there  is  a  tendency  to  '  bronchitis  ',  opium  being  contra-indicated 
in  the  latter  class  because  of  its  tendency  to  prevent  the  free  expulsion 
of  the  phlegm. 

Among  more  neurotic  patients  I  have  found  bromide  of  ammonium 
of  inestimable  service,  not  only  in  inducing  sleep,  but  in  keeping  the  mind 
from  worrying,  and  in  inducing  a  lethargy  that  is  beneficial  to  the  heart. 
Even  in  severe  cases  of  angina  pectoris  I  have  found  it  of  great  value.  Thus, 
a  lady  with  aortic  valvular  disease,  between  the  age  of  fifty  and  sixty, 
became  liable  to  attacks  of  angina  pectoris.  At  times  these  were  so  severe 
that  she  was  forced  to  lie  in  bed.  The  exhaustion  of  the  heart  was  so  great 
that  the  sounds  were  sometimes  scarcely  perceptible.  After  a  period  of 
rest  the  heart  regained  strength  and  she  was  able  to  go  about,  collapsing, 
however,  again  and  again  after  a  few  months.  On  making  minute  inquiry 
into  the  cause  of  these  attacks,  I  found  that  she  suffered  from  sleeplessness 
for  a  week  or  two  prior  to  a  breakdown.  I  therefore  prescribed  bromide 
of  ammonium,  20  grains  three  times  a  day,  during  one  of  her  attacks  of 
heart  failure.  In  a  few  days  she  got  quiet  sleep  and  speedily  recovered. 
When  she  began  to  experience  a  restless  night  she  resorted  to  the  bromide, 
and  it  never  failed  to  give  her  sleep,  and  no  doubt  warded  off  the  attack, 
for  on  several  occasions  she  neglected  the  medicine  and  after  a  few  sleepless 
nights  the  attack  of  angina  pectoris  returned. 

The  good  effects  of  the  bromide  in  nervous  cases  have  been  referred  to  in 
Chapter  VIII.  The  dose  of  the  various  hypnotics  varies  with  each  patient. 
Small  doses  should  be  used  at  first,  and  the  drug  pushed  carefully  and 
steadily  till  some  effect  is  produced.  Repeated  doses  every  one  or  two  hours 
should  be  tried  at  first. 

§  243.  Bodily  comfort — In  cases  of  severe  heart  failure  much  can  be 
done  by  removing  all  sources  of  discomfort.    Detailed  instructions  regarding 


TREATMENT  271 

sponging  the  body  and  arranging  the  bed  so  that  the  patient  lies  com- 
fortably with  light  and  warm  bedclothes  should  be  given  ;  too  great 
warmth  should  be  avoided.  The  patient  often  wishes  to  assume  some 
position  that  the  attendant  may  fancy  to  be  harmful,  but  his  inclination 
should  be  complied  with  and  everything  done  to  keep  him  comfortable  in 
the  position  assumed,  as  with  the  shoulders  raised,  sitting  upright,  or  bending 
forward  with  the  head  supported.  He  may  prefer  sitting  in  a  chair  with 
his  arms  on  a  table  and  his  head  resting  on  them.  In  all  these  positions  he 
is  instinctively  assuming  a  position  that  helps  the  heart  in  its  work.  In  all 
cases,  mild  or  severe,  every  source  of  discomfort  from  other  parts  of  the 
body  should  be  attended  to,  such  as  an  irritating  skin  affection,  piles, 
frequent  micturition. 

§  244.  Diet. — In  calculating  the  results  obtained  by  any  mechanical 
process  it  is  necessary  to  understand  all  the  factors  concerned.  The  neglect 
of  one  factor  necessarily  vitiates  the  calculation.  Because  of  the  slight 
advance  in  biochemistry  many  attempts  have  been  made  to  find  a  scientific 
dietary.  But  as  the  factors  concerned  in  metabolism  are  as  yet  imperfectly 
understood,  it  is  manifestly  hopeless  to  base  a  dietary  on  knowledge  that 
does  not  include  all  the  factors  concerned.  Notwithstanding  the  confident 
assertion  of  many  dietetic  authorities,  the  perfect  dietary  has  yet  to  be 
evolved,  and  in  the  meantime  we  must  be  content  to  be  guided  by  common 
sense  and  experience. 

In  cases  of  heart  failure  a  good  deal  of  harm  can  be  done  by  injudicious 
feeding.  It  must  be  kept  in  mind  that  in  extreme  heart  failure  and  in  febrile 
cases  the  digestive  functions  are  themselves  greatly  weakened,  and  that  to 
pour  food  into  a  weakened  stomach  is  not  only  to  add  to  the  discomfort  of 
the  patient,  but  may  produce  flatulent  distension  of  the  stomach  and  bowels, 
which,  pressing  on  the  diaphragm,  embarrasses  the  heart  and  respiration.  The 
manifest  weakness  of  the  patient  is  often  taken  as  an  indication  for  more 
food  to  restore  the  strength,  and  satisfaction  is  felt  so  long  as  fluid  is  seen  to 
disappear  into  the  patient's  interior.  It  is  very  curious  how  prevalent  the 
custom  is,  when  the  stomach  is  weak,  to  give  it  more  work  to  do.  The  food 
is  prepared  in  such  a  manner  that  the  assistance  of  the  mouth  is  dispensed 
with,  and  more  work  is  therefore  thrown  upon  the  stomach.  Bread  and 
milk,  a  favourite  food,  is  so  prepared  that  no  mastication  is  needed,  and  the 
stomach  is  burdened  with  the  duty  of  getting  rid  of  the  load.  The  great 
importance  of  oral  digestion  is  not  sufficiently  appreciated.  Not  only  does 
the  process  of  mastication  in  several  subtle  ways  stimulate  the  digestive 
glands  of  other  organs,  but  the  juices  from  the  mouth  that  are  mixed  with 
the  food  not  only  assist  digestion  but  prevent  the  flatulence  which  is  so  often 


272  DISEASES  OF  THE  HEART 

such  a  troublesome  feature  in  the  weakened  digestion  of  heart  failure.  I  wish 
to  insist  upon  this  all  the  more  as  it  is  becoming  more  and  more  the  vogue 
to  give  patients  partially  digested  foods,  or  foods  supposed  to  be  prepared  to 
make  digestion  easier,  and,  relying  upon  the  notion  that  digestion  is  being 
assisted,  the  physician  is  apt  to  ignore  the  natural  and  infinitely  better 
methods  provided  by  nature.  These  short  cuts  to  treatment  are  invariably 
in  the  end  bad  for  patient  and  physician — leading  the  latter  to  a  rule-of- 
thumb  practice,  neglecting  thereby  to  make  of  each  individual  a  special 
study. 

In  cases  of  extreme  heart  failure,  with  dropsy,  the  food  should  be  very 
limited  in  quantity — as  a  rule,  small  quantities  of  milk  given  at  frequent 
intervals,  in  extreme  cases  not  more  than  one  pint  per  day.  The  patient 
should  be  encouraged  to  take  a  small  portion  of  biscuit,  or  a  dainty  sandwich 
with  fresh  potted  meat,  chewed  very  thoroughly.  In  febrile  cases,  or  when 
the  mouth  tends  to  become  dirty,  it  should  be  washed  or  sponged  out,  and 
immediately  afterwards  a  smaU  piece  of  solid  food  should  be  given  to  chew. 
The  quantities  should  always  be  smaU,  so  that  the  patient  is  not  nauseated 
by  the  spectacle  of  an  untempting  quantity  of  food. 

With  less  severe  cases  the  food  should  be  more  varied,  but  it  should 
never  be  forced  on  the  patient.  The  quantity  he  can  chew  is  often  a  very 
good  guide,  because  if  he  cannot  be  tempted  to  chew  much  it  is  manifest 
his  digestive  functions  are  at  fault,  and  it  is  a  very  bad  practice  in  such  cases 
to  pour  in  beef-tea  and  other  easily  eliminated  fluids.  The  guiding  principle 
should  be  food,  tempting,  needing  mastication,  with  Kttle  fluid,  and  that 
chiefly  milk,  given  smaU  in  quantity  and  at  fairly  frequent  intervals — the 
intervals  depending  on  the  quantity  he  is  able  to  take.  The  kind  of  food 
should  be  that  which  the  patient  hkes,  so  long  as  it  does  not  disagree  with 
him.  The  doctor  must  be  on  his  guard  not  to  prescribe  a  dietary  suitable 
to  himself,  but  must  bear  in  mind  that  what  disagrees  with  him  may  agree 
with  his  patient.  In  selecting  a  dietary  the  resources  of  an  inteUigent 
housewife  wiU  often  be  found  to  be  of  much  service. 

Individuals  with  heart  trouble,  but  able  to  get  about,  should  lead  a  hfe  of 
abstemiousness,  avoiding  aU  excesses.  The  meals  should  be  small  in  quantity, 
and  of  such  frequency  that  faintness  is  avoided.  It  often  happens  that  they 
become  faint  in  the  night,  or  early  in  the  morning,  as  they  have  not  broken 
their  fast  since  the  evening  meal.  A  dry  biscuit  and  a  smaU  cup  of  milk 
at  bedtime  or  in  the  early  morning  wiU  often  prevent  the  occurrence  of 
disagreeable  sensations. 

A  class  of  people  for  whom  many  dietaries  have  been  evolved  are  those 
who  with  advancing  years  show  some  signs  of  wear  and  tear.    It  may  be  that 


TREATMENT  273 

in  their  vigorous  manliood  they  enjoyed  and  gratified  excellent  appetites, 
but  as  the  years  begin  to  tell  the  pleasures  of  the  table  no  longer  appeal 
to  them.  Signs  of  the  heart  faihng  may  manifest  themselves,  and  the 
individual  begins  to  take  thought  and  seeks  advice.  Such  a  one  readily 
becomes  the  victim  of  a  dietetic  craze.  A  course  of  life  that  seems  to  put 
back  the  hand  of  time  appeals  to  him.  As  one  who  has  watched  many  of 
these  patients  over  periods  of  many  years,  I  have  seen  no  evidence  which 
convinces  me  that  the  various  abstemious  dietaries  that  I  have  tried  and 
seen  others  try  arrest  the  progress  of  senility.  With  advance  of  years  the 
appetite  diminishes  as  a  rule,  and  this  is  good,  as  the  process  of  assimilation 
also  becomes  enfeebled.  While  moderation  in  all  things  is  good,  it  is  difficult 
to  tell  what  are  its  hmits. 

In  some  of  my  cardio-sclerotic  patients  the  appetite  has  been  maintained 
with  remarkable  keenness.  I  have  seen  such  patients  becoming  seriously 
crippled  through  failure  of  the  heart,  with  the  nodal  rhythm,  very  high 
blood-pressure,  and  sweUing  in  the  legs.  I  have  endeavoured  to  restrain  their 
appetite  and  to  restrict  their  diet,  but  have  only  succeeded  in  increasing  their 
weakness  and  making  them  miserable.  With  the  resumption  of  their  old 
dietary  I  have  seen  them  improve,  and  glide  gently  past  the  threescore  years 
and  ten  and  well  on  to  the  fourscore  years  before  they  passed  away  with 
little  suffering.  To  the  dyspeptic,  asceticism  may  appear  an  ennobling 
creed,  but,  as  a  practical  physician  doing  my  best  for  my  patients,  I  think 
I  would  rather  see  my  patients  passing  the  declining  years  in  comfort,  even 
though  their  chief  pleasures  were  those  of  the  table,  than  having  their  lives 
made  tedious  and  uninteresting  through  depriving  them  of  that  which  gives 
them  pleasure  in  the  hope  of  adding  a  few  months  to  their  existence. 

I  must  also  add  a  warning  to  those  who  may  imagine  they  can  modify 
changes  in  the  heart  and  blood-vessels  by  the  elimination  of  certain 
constituents  of  food,  as  common  salt.  I  have  seen  patients  made  neurotic 
and  apprehensive  because  a  physician  had  warned  them  of  the  evils  of 
common  salt,  so  that  they  were  made  conscious  of  their  ailment  at  each 
meal,  and  were  filled  with  dread  lest  their  food  should  contain  salt.  The 
domestic  comfort  of  a  whole  household  may  be  jeopardized  by  having  to 
cook  the  food  free  from  salt,  and  all  the  members  are  made  to  suffer  because 
of  this  foohsh  restriction.  This  does  not  apply  to  patients  seriously  ill, 
when,  for  the  removal  of  dropsy,  a  special  invahd  dietary,  salt-free,  may 
be  tried.  The  same  foohsh  notion  exists  in  regard  to  lime,  the  notion 
being  that  hme  salts  can  be  removed  from  the  tissues  by  decalcifying  agents, 
or  prevented  from  being  deposited  by  restricting  the  Hme  contents  of  the 
food.     Calcium  given  by  the  mouth  is  absorbed  very  slowly  and  only   to 

MACKENZIE  m 


274  DISEASES  OF  THE  HEART 

a  slight  extent,  and  is  as  rapidly  excreted,  while  decalcifying  agents  like 
citric  acid  have  no  appreciable  effect. 

§  245.  The  condition  of  the  bowels — The  condition  of  the  bowels 
should  be  attended  to  in  every  case.  Constipation  and  straining  at  stool 
may  produce  great  exhaustion.  In  the  less  severe  cases  of  heart  affections 
the  habit  of  going  regularly  to  the  closet  and  patiently  waiting  wiU  sometimes 
be  effectual.  When  the  bowels  are  more  stubborn,  aperients  are  necessary. 
The  various  mineral  waters  are  beneficial,  but  where  the  expense  is  a  con- 
sideration simpler  remedies  can  be  usefuUy  substituted,  as  a  smaU  quantity 
of  Epsom  salts  in  a  tumbler  of  hot  water  every  morning,  or  a  teaspoonful  of 
compound  Hquorice  powder  in  a  tumbler  of  water  at  bedtime.  A  pill 
containing  |  grain  each  of  extract  of  belladonna,  extract  of  nux  vomica,  and 
aloin,  taken  three  times  a  day,  is  in  many  cases  extremely  useful.  In  more 
stubborn  cases  enemata  may  have  to  be  resorted  to — a  pint  of  soap  and 
water  given  at  night. 

Treatment  by  purgatives  is  often  helpful  in  cases  where  there  is  much 
congestion  of  the  Uver  and  abdominal  stasis,  and  scanty  flow  of  urine.  A  free 
evacuation  can  be  obtained  by  any  of  the  purgatives,  such  as  the  coloc3mth 
and  hyoscyamus  piU,  calomel,  or  blue  pills.  After  the  free  evacuation  of  the 
bowels,  they  should  be  kept  open  by  some  milder  aperient. 

In  all  these  cases  care  must  be  observed  that  the  patient  is  not  too  greatly 
exhausted  by  the  movement  of  the  bowels,  for  it  is  sometimes  surprising  how 
prostrate  some  patients  become  after  the  bowels  are  moved.  An  enema 
may  prevent  straining,  but  if  the  exhaustion  is  too  extreme,  the  bowels  had 
better  be  left  alone. 

§  246.  The  mental  factor — The  consciousness  of  heart  trouble  has 
often  a  depressing  effect  upon  people,  whether  the  trouble  be  shght  or  serious. 
When  such  people  become  convinced  that  the  trouble  is  curable  or  not  serious, 
their  condition  at  once  becomes  greatly  improved.  Cures  by  faith,  whether 
in  drugs,  baths,  elaborate  methods,  or  religion,  act  by  playing  upon  the 
mental  condition.  I  have  already  said  that  we  should  always  study  the 
mental  condition  of  the  patient,  and  its  bearing  upon  his  complaint,  and 
we  should  utilize  its  peculiar  features  in  treatment.  But  our  employment  of 
this  element  in  treatment  should  not  be  the  outcome  of  blind  unreasoning 
faith  in  some  rite  or  ceremony,  bath  or  drug,  but  in  the  intelligent 
perception  of  the  nature  of  the  symptom.  The  reassurance  of  the  patient 
of  the  harmless  nature  of  the  complaint  goes  a  great  way  in  curing  him. 
When  there  is  some  affection  that  cripples  him,  the  reassurance  that  with 
reasonable  care  no  danger  need  be  feared  is  extremely  helpful.  Even  in 
serious   cases,   when   there  is  reasonable   hope   of  recovery,  or   a   certain 


TREATMENT  275 

degree  of  recovery,  the  encouragement  of  the  patient  may  and  does   help 
forward  his  improvement. 

This  mental  factor  should,  on  the  other  hand,  make  us  extremely  chary 
of  giving  the  patient  a  gloomy  prognosis.  There  is  nothing  in  my  ex- 
perience so  surprising  as  the  manner  in  which  the  heart  can  recover  from 
the  seemingly  most  hopeless  condition  of  exhaustion.  And  we  must  bear  in 
mind  that  a  gloomy  view  may  in  itself  nullify  the  best  attempts  at  treatment. 
We  should  aim  at  getting  the  patient  into  a  placid,  contented,  hopeful  frame 
of  mind,  so  that  the  heart  is  not  disturbed  by  emotional  reflexes. 

§  247.  Drugs. — The  influence  of  drugs  upon  the  heart  is  one  to  which 
I  have  given  a  good  deal  of  attention,  and  I  have  carried  out  a  long  series 
of  observations  with  many  of  those  most  commonly  employed  in  practice. 
The  subject  is  one  that  needs  a  great  deal  more  elucidation,  and  I  give  here 
the  results  of  my  observations  so  far. 

Many  drugs  have  a  reputation  for  the  good  effect  they  have  upon  the 
heart,  but  I  found  very  little  evidence  of  their  beneficial  action.  An  exception 
to  this,  however,  was  found  in  the  case  of  the  digitalis  group,  but  even  here 
the  manner  of  action  and  the  cases  suitable  for  treatment  have  never  been 
clearly  described,  so  that  a  great  portion  of  my  observations  were  devoted 
to  finding  out  how  the  drug  acts  and  how  it  should  be  used.  The  results 
obtained  are  so  important  that  I  give  an  outline  of  them  in  Chapter  XXXIV, 
with  a  fuller  illustration  of  some  particular  instances  in  the  Appendix  (VI). 

The  class  of  drugs,  apart  from  digitalis,  that  I  found  having  a  more  or  less 
demonstrable  effect  upon  the  heart  were  the  vaso-dilators.  Every  one 
knows  and  appreciates  the  effect  that  the  inhalation  of  the  nitrite  of  amyl 
has  upon  the  peripheral  circulation.  But  although  its  evidence  is  so  demon- 
strable, I  am  not  at  all  sure  how  it  acts  beneficially  upon  the  heart.  The 
most  obvious  explanation  is  not  necessarily  the  true  one.  I  have  already 
expressed  my  doubts  as  to  the  correctness  of  the  explanation  of  its  action 
in  angina  pectoris  (§  58).  The  usual  explanation  is  that  there  is  an  arterial 
spasm  which  offers  great  resistance  to  the  heart,  and  the  amyl  nitrite  relieves 
the  spasm.  There  can  be  no  doubt  but  that  the  rehef  obtained  by  many 
people  during  attacks  of  angina  pectoris  where  there  is  high  blood-pressure 
by  means  of  amyl  nitrite  or  trinitrin,  may  be  due  to  lowering  of  the  blood- 
pressure,  but  there  are  other  cases  in  which  the  drugs  give  relief  where 
there  is  no  arterial  spasm,  and  if  the  arterial  pressure  be  taken  as  the  measure 
of  the  spasm,  it  will  be  found  that  a  few  minutes  after  the  effect  of  the  amyl 
nitrite  has  passed  off  the  arterial  pressure  may  be  greatly  raised. 

The  employment  of  other  nitrites,  as  nitro-glycerine,  to  reduce  per- 
manently high  arterial  pressure,  has  been  in  my  hands  of  very  Uttle  avail, 

t2 


27&  DISEASES  OF  THE  HEART 

though  I  have  persevered  with  the  drug  for  considerable  periods.  The 
action  of  the  nitrites  is,  as  a  rule,  transient,  and  they  seem  to  have  little 
lasting  effect.  I  am  now  of  opinion  that  in  high  pressures,  with  degenerated 
arteries  and  a  diminished  capillary  field,  they  are  useless.  Even  if  they 
acted  as  permanent  vaso-dilators,  I  doubt  if  their  use  would  be  justified 
in  cases  of  high  arterial  pressure.  Besides,  one  often  notices  that  when  by 
any  means  the  high  pressure  is  reduced,  the  patient  is  certainly  no  better, 
but  often  weaker. 

In  cases  of  high  arterial  pressure,  with  a  good  deal  of  discomfort,  as 
pain  and  tightness  across  the  chest,  iodide  of  potassium  has  a  great  reputa- 
tion, which  has  been  justified  in  my  experience.  I  have  also  used  it  with 
seemingly  good  results  in  elderly  patients  with  recurrent  attacks  of  bronchitis. 
At  one  time  I  thought  it  acted  by  lowering  the  pressure,  but  I  found  the  good 
results  occur  with  no  alteration  in  the  pressure.  I  have  not  used  the  large 
doses  sometimes  recommended,  but  5  grains  three  or  four  times  a  day. 
These  doses  rarely  produce  iodism. 

I  have  been  struck  with  the  good  effects  of  chloral  in  some  of  these  cases 
of  high  blood-pressure,  given  in  small  doses  (5  grains)  two  or  three  times 
a  day,  as  well  as  in  larger  doses  to  induce  sleep.  Many  of  my  patients  who 
suffered  from  severe  attacks  of  angina  pectoris  found  chloral  gave  them  the 
greatest  relief,  and  some  used  to  carry  it  when  liable  to  these  attacks.  The 
attacks  did  not  come  on  with  sudden  violence,  but  gradually  after  exertion, 
and  the  chloral  often  gave  complete  relief  in  about  ten  minutes. 

The  vaso-constrictors  have  been  of  little  use  in  my  hands.  I  have 
repeatedly  used  adrenalin  in  cases  of  low  arterial  pressure,  but  it  never  pro- 
duced any  effect  that  led  me  to  look  upon  it  as  of  much  value.  A  number  of 
drugs  apart  from  the  digitalis  group  have  a  reputation  as  '  cardiac  tonics  ', 
but  I  could  never  find  any  evidence  of  their  effect  upon  the  heart,  beyond 
that  indefinite  beneficial  tonic  effect  that  follows  the  administration  of  such 
drugs  as  quinine.  The  most  popular  remedy  of  this  class  is  strychnine,  or 
some  preparation  of  nux  vomica.  I  have  carefully  sought  for  its  special 
i  effect  on  the  heart  and  found  none.  When  I  inquired  into  the  evidence  for 
jits  supposed  good  effect,  I  found  that  it  was  practically  all  clinical,  and 
clinical  evidence  endows  the  drug  with  the  most  diverse  properties.  It  is 
recommended  as  a  cardiac  stimulant  in  slow-acting  hearts,  and  even  in 
heart-block  it  is  said  to  quicken  the  beat.  It  is  also  recommended  in  the 
too-excitable  heart,  as  when  there  are  extra-systoles,  and  in  the  rapid  heart 
of  acute  myocardial  affections.  It  is  said  to  be  beneficial  in  cases  of  low 
blood-pressure,  and  equally  beneficial  in  cases  of  high  tension,  and  even  in 
angina  pectoris.    The  evidence  that  can  show  a  drug  to  possess  the  property 


TREATMENT 


277 


of  exciting  the  sluggish  and  of  soothing  the  excited,  of  raising  the  low 
pressure  and  reUeving  the  high,  speaks  more  for  unreasoning  faith  in  the 
drug  than  for  the  beneficial  properties  of  the  drug  itself. 

Since  this  was  written,  Professor  W.  E.  Dixon  392,  in  an  address  before  the 
—  '  '  ""'  ■        "   'e  British  Medical  Association, 

e)  are  still  employed  on  the 
^ased  activity.     The  effect  of 
e  doses  it  tends  to  depress 
never  excites.     Strychnine 
art  ;   by  exciting  the  vaso- 
)-motor  activity  indirectly, 
jry  with  digitalis,  lead,  and 

Inst  placing  trust  in  drugs  to 
nt.     There  is  a  very  common 
heart,  not  to  the  rest  that  it 
thod  employed.     This  is  hke 
who  is  restored  by  a  plate  of 
'«soup  is  flavoured, 
'n  is  invaded  by  some  organism, 
pe  of  effective  treatment,  but  of 
(leumatic  affection  of  the  heart, 
^  oy  great  benefit.     These  should, 
'  3  not  used  them  frequently  in 
tiave  seen  such  good  results  that 
trial.     He  has  kindly  written  out 
employs  in  giving  large  doses  of 


N  OF  SODIUM  SALICYLATE 

ie  and  subacute  rheumatism  and  of 
te  are  often  necessary.  In  spite  of 
jleasant  symptoms,  such  as  vomitmg, 
ile  to  give  large  doses,  if  the  following 

cylate,  twice  as  much  Sodium  Bicar- 

-^■^^  given  every  two  hours  during  the  day 
night  :   ten  doses  in  twenty-four  hours. 
GREATEST     PLEASURE  symptoms  are  produced    two  ^J  ^^ree  dose^ 
n  XT     T-  H  T7     \T7  T7   G  T-       the   administration  should  be  recommencea, 
UN       IHbVVEST  one-half,  or    two-thirds  of    the  previous  dose. 


276 


DISEASES  OF  THE  HEART 


though  I  have  persevered  with  the  drug  for  considerable  periods.  The 
action  of  the  nitrites  is,  as  a  rule,  transient,  and  they  seem  to  have  little 
lasting  effect.  I  am  now  of  opinion  that  in  high  pressures,  with  degenerated 
arteries  and  a  diminished  capillary  field,  they  are  useless.  Even  if  they 
acted  as  permanent  vaso-dil 

in  cases  of  high  arterial  pres^ 

any  means  the  high  pressure 
but  often  weaker. 

In  cases  of  high  arteri 
pain  and  tightness  across  t 


VEXICE 


tion,  which  has  been  justify? 
seemingly  good  results  in  elde 


12  15 
12  33 
12  47 
12  53 
I  07 
I  15 
I  19 


12  45 
I  08 
I  17 
I  23 
I  37 
I  45 
I   49 


I  1511  45|2  I5|2  4513  151 
I  38|2  08|2  38|3  08|3  34| 
I   4712   I7|2  4713   1713  451 


1  5312  23 

2  0712  37 
2  15  2  45 
2   19  2  49 


2  5313  23]3  531. 

3  07  3  3714  071. 
3  15  3  45  4  15  . 
3  I9|3  49|4  I9|. 


At  one  time  I  thought  it  actecno  15110  45] n 


*S    I    ♦S    1 

-1- 


II    I51II   45|12  15112  45  1  15 

10  38111    08[ll    38|l2  08  12  38    1  08  1  38 

results  occur  with  no  alteratii!|g  ^^|||  ^^i!l  Unl  2^1;:::: :::::  1 57 

,  .  ,'111    07|ll   37112  07112  37 | 2  07 

sometimes  recommencf!"  'si"  45112 15112  451 1 12 15 

11  I9III   49112  19112  401 I I---- 

LOS   ANGELES 


doses 

These  doses  rarely  produce  i<' 
I  have  been  struck  with  tl- 
of  high  blood-pressure,  given 

a  day,  as  well  as  m  larger  dose?^|l|  ^^i  I  ?^'l  ^l  Itl  ^^  Vz\l  It 
suffered  from  severe  attacks  ofl'^lTlf'm^^^—^ 


;ni|2  00112  30!l  OOil  3012  0012  30|3  00 

!4!|2  04112  34il  04!  I  34|2  04i2  34.3  04 

12    12  12  42  I  12  I  42  2  1212  42|3  12 

12  26il2  56i|  26  I  56i2  2612  5613  26 


10  34 
10  42 

10  56 

11  04 
II    13 


I  04 
II  12 
II    26 


1 1   36112  06112  361. 


greatest  relief,  and  some  used  tc  oono  301  n  00 

04 "    "■ 

attacks  did  not  come  on  with  si  26 
and  the  chloral  often  gave  comp*? 

The  vaso-constrictors  have 
repeatedly  used  adrenalin  in  case  ■ 
duced  any  effect  that  led  me  to  lo» 
drugs  apart  from  the  digitalis  groj 
but  I  could  never  find  any  evidenv' 
that  indefinite  beneficial  tonic  effec 
I  drugs  as  quinine.     The  most  popul  "^1°" 


II  30112.00 

II  34]12  04 

I  I  42I12  12 

II  56112  28 
II   34112  04112  34 

4311 


1  00 
1  04 
1  12 
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1  34 


■U'estgate,  Brentwood  and  Palisades. 


LAUREL   CANYON 


gil  iG 
ell  31 
gll  40 
cl2  01 
gl2  16 
gl2  31 
gl2  46 


some  preparation  of  nux  vomica.  K"'-'-''- 
effect  on  the  heart  and  found  none.  \  j^^ 

I  found  th"9  33 

9  45 

03 
15 
33 


LOS      ANGELES 


cU  45 

12  ()?. 
gl  20 


,  its  supposed  good  effect 
j  clinical  evidence  endows  the  drug  wi 
I  recommended  as  a  cardiac  stimulant., 
heart-block  it  is  said  to  quicken  the  be, 
too-excitable  heart,  as  when  there  are  exti 

of  acute  myocardial  affections.     It  is  said  .      

blood-pressure,  and  equally  beneficial  in  cases" 
angina  pectoris.    The  evidence  that  can  show  a  dru 


WESTERN  AND  FRANKLIN 
AVE.    LINE 

Los  Angeles  —  Via  Sanborn, 
Santa  Monica  Blvd.,  Western 
and  Franldin  Ave.,  to  Vine 
St.,  HoUy^vood 


LOS  ANGELES   ! 

HOLLYWOOD 

Hill  St. 

Station 

Vine 

Street 

U  40 

12  46 

6  05 

12  05 

7  16 

1  16 

6  o5 

12  35 

7  46 

1  46 

7  05 

1  05 

8  16 

2  16 

7  35 

1  35 

8  46 

2  46 

8  05 

2  05 

9  16 

3  16 

8  35 

2  35 

9  46 

3  46 

9  05 

3  05 

10  16 

4  16 

9  35 

3  35 

10  46 

4  46 

10  05 

4  05 

11  16 

5  16 

10  35 

4  35 

11  46 

5  46 

11  05 

5  05 

12  16 

6  16 

11  35 

5  35 

Connects   with   Brush   Canyon  Line. 
All   trains  daily. 


COLEGROVE,    CRESCENT 

JCT.    AND    SHERMAN 

LINE 

LOS  ANGELES  (Hill  St.  Sta- 
tion) to  Colegrove,  Crescent 
Jet.  and  Sherman 


■N*4  00 

*10  56 

Its  06 

t7  16 

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lltl2  06 

♦4  26 

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♦7  56 

♦12  26 

llt4  36 

t9  16 

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lltl2  36 

♦4  56 

t9  36 

*8  26 

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JtS  06 

♦9  56 

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tlO  16 

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niO  06 

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t6  36 

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*10  26 

♦2  56 

♦6  56 

♦12  40 

tltlO  36 

SHERMAN,    Crescent   Jet.    and 
Colegrove  to   Los    Angeles 


♦5  11 

HtlO  28 

♦2  41 

t7  16 

♦5  41 

♦10  41 

IIt2  58 

t7  36 

♦6  11 

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♦3  II 

t7  56 

♦6  41 

•11  11 

lit3  28 

t8  16 

lite  58 

Ull  28 

♦3  41 

t8  36 

♦7  11 

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11 13  58 

18  56 

lit7  28 

litll  58 

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t9  16 

♦7  41 

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llt7  58 

lit  12  28 

♦4  41 

t9  56 

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HtS  28 

lltl2  58 

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tlO  36 

♦8  41 

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llt5  28 

tlO  56 

HtS  58 

Htl  28 

♦5  41 

til  16 

♦9  11 

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til  36 

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fitl  58 

t6  16 

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♦9  41 

♦2  II 

t6  36 

Htn  58 

llt2  28 

ta  56 

♦10  11 



■jiXaioi^^as    SxVoixvaoitK033V 


TREATMENT  277 

of  exciting  the  sluggish  and  of  soothing  the  excited,  of  raising  the  low 
pressure  and  reheving  the  high,  speaks  more  for  unreasoning  faith  in  the 
drug  than  for  the  beneficial  properties  of  the  drug  itself. 

Since  this  was  written.  Professor  W.  E.  Dixon  ^^^^  [^  an  address  before  the 
section  of  Pharmacology  and  Therapeutics  of  the  British  Medical  Association, 
said:  'Both  these  drugs  (ether  and  strychnine)  are  still  employed  on  the 
supposition  that  they  excite  the  heart  to  increased  activity.  The  effect  of 
ether  is  to  depress  nerve-tissues  ;  in  very  large  doses  it  tends  to  depress 
muscle-tissue,  including  cardiac  muscle,  but  it  never  excites.  Strychnine 
likewise  has  no  direct  stimulant  action  on  the  heart  ;  by  exciting  the  vaso- 
motor centre  it  may  sUghtly  increase  the  vaso-motor  activity  indirectly, 
but  it  should  never  be  put  in  the  same  category  with  digitahs,  lead,  and 
other  cardiac  drugs.' 

The  reason  I  dwell  upon  this  is  to  warn  against  placing  trust  in  drugs  to 
the  neglect  of  the  essential  requisite  in  treatment.  There  is  a  very  common 
tendency  to  attribute  the  improvement  in  the  heart,  not  to  the  rest  that  it 
has  obtained,  but  to  the  special  drug  or  method  employed.  This  is  hke 
attributing  the  recovery  of  a  famishing  man  who  is  restored  by  a  plate  of 
nourishing  soup  to  the  garhc  with  which  the  soup  is  flavoured. 

In  acute  febrile  conditions,  when  the  heart  is  invaded  by  some  organism, 
vaccine  or  serum  therapy  holds  out  some  hope  of  effective  treatment,  but  of 
this  I  have  had  no  experience.  In  acute  rheumatic  affection  of  the  heart, 
the  use  of  the  salicylates  is  often  attended  by  great  benefit.  These  should, 
however,  be  pushed,  and,  though  I  have  not  used  them  frequently  in 
the  manner  recommended  by  Lees,  yet  I  have  seen  such  good  results  that 
I  think  Lees's  method  should  be  given  a  trial.  He  has  kindly  written  out 
for  me  the  directions  and  precautions  he  employs  in  giving  large  doses  of 
salicylate  of  soda  : — 

NOTE  ON  THE  ADMINISTRATION  OF  SODIUM  SALICYLATE 

For  the  effective  treatment  of  acute  and  subacute  rheumatism  and  of 
chorea,  large  doses  of  Sodium  SaUcylate  are  often  necessary.  In  spite  of 
the  tendency  of  this  drug  to  produce  unpleasant  symptoms,  such  as  vomiting, 
deafness,  &c.,  it  is  almost  always  possible  to  give  large  doses,  if  the  following 
method  of  administration  be  adopted  : — 

(1)  To  every  dose  of  Sodium  Sahcylate,  twice  as  much  Sodium  Bicar- 
bonate must  be  added. 

(2)  The  combined  drugs  must  be  given  every  two  hours  during  the  day 
and  every  four  hours  during  the  night  :   ten  doses  in  twenty-four  hours. 

(3)  When  any  unpleasant  symptoms  are  produced,  two  or  three  doses 
should  be  omitted.  Then  the  administration  should  be  recommenced, 
using    smaller    amounts  ;    one-half,  or    two-thirds  of   the  previous  dose, 


278  DISEASES  OF  THE  HEART 

according  to  circumstances,  but   given  as   before  ten    times   daily.      The 
amount  should  then  be  increased  as  rapidly  as  possible. 

(4)  The  initial  dose  may  be  15  grains  for  an  adult,  10  grains  for  a  child 
of  8-12  years,  5  grains  for  a  younger  child.     This  amounts  to — 

150  grains  Sod.  Sal.  with  300  grains  Sod.  Bicarb,  daily 

lUU         ,,  ,,  ,,  ,,      ^\J\j         ,,  ,,  ,,  ,, 

"'-'  ))  5  5  5  5  5  5  iUU  ,,  ,,  ,,  ,, 

(5)  The  amount  of  these  drugs  should  be  increased  every  day,  or  every 
second  day,  by  5  grains  of  Sod.  Sal.  and  10  grains  of  Sod.  Bicarb,  in  each 
dose,  or  daily  50  and  100  grains  respectively. 

(6)  The  administration  should  be  temporarily  suspended  if  vomiting, 
deafness,  tinnitus,  or  any  tendency  to  delirium  be  produced.  But  the 
period  of  suspension  should  be  short — rarely  more  than  12  hours — often 
a  shorter  period  suffices  if  the  amount  given  be  reduced. 

(7)  The  amount  of  Sodium  Salicylate  required  in  ordinary  acute  rheu- 
matism is  from  100  to  250  grains  daily  ;  in  chorea  from  200  to  350  grains  ; 
in  chronic  subacute  rheumatism  the  dose  may  require  to  be  raised  to  450 
grains  or  even  500  grains. 

(8)  Children  require  nearly  as  large  doses  as  adults,  for  in  them  the 
rheumatic  infection  is  specially  virulent. 

(9)  Enough  Sodium  Bicarbonate  must  be  employed  to  render  the  urine 
alkaline.  If  this  be  secured,  and  constipation  be  prevented,  the  Salicylate 
may  be  given  freely  without  apprehension.  But  if  a  rheumatic  child  be 
costive  and  too  little  bicarbonate  be  given,  it  is  possible  to  bring  about  a 
condition  of  poisoning  by  Salicylate — drowsiness,  and  deep  breathing,  in- 
creasing to  air  hunger  and  coma,  with  acetonuria  and  the  odour  of  acetone 
in  the  breath.  This  is  the  real  danger  from  Salicylate  ;  it  may  also  be  pro- 
duced by  aspirin.  But  it  can  always  be  avoided  by  attention  to  the  direc- 
tions given  above.  The  existence  of  this  danger  should  make  the  physician 
watchful,  but  it  should  not  lead  him  to  deprive  the  patient  of  the  great  benefit 
to  be  obtained  from  large  doses  of  the  drug. 

§  248.  Oxygen. — Although  oxygen  has  been  employed  for  many 
years  in  affections  of  the  heart  and  lungs,  it  must  be  confessed  that  its 
employment  has  not  been  followed  by  the  good  results  which  were  hoped 
for.  Every  one  who  has  used  it  to  any  extent  in  affections  of  the  heart 
has  found  it  of  distinct  advantage  in  exceptional  cases,  but  on  the  whole 
the  results  have  been  disappointing.  In  a  measure  it  may  be  that  this 
disappointment  was  due  to  two  things,  (1)  that  there  are  only  certain  cases 
suitable  for  this  oxygen  treatment,  (2)  that  it  has  not  been  given  in  sufficient 
amount. 

To  take  the  second  of  these  suggestions  first,  I  was  impressed  with  the 
observations  of  Hill  and  Flack  *°2,  whose  experimental  work  demonstrated 
that  oxygen  relieved  the  strain  on  the  athlete's  heart,  and  that  by  the 
somewhat  open  method  usually  employed  there  was  not  sufficient  con- 
centration of  the  oxygen  inhaled.     Thus  Hill  and  Flack  found  that  the 


TREATMENT  279 

percentage  of  oxygen  inhaled  in  the  ordinary  open  method  by  a  funnel 
was  19-27  per  cent,  in  the  alveolar  air,  whereas  by  the  method  described 
below  there  was  over  70  per  cent,  of  oxygen  in  the  alveolar  air. 

In  regard  to  the  cases  suitable  for  oxygen,  slight  temporary  relief  is 
obtained  by  all  cases  that  are  more  or  less  cyanotic.  I  had  hoped,  however, 
that  it  would  have  proved  useful  in  another  class  of  case  where  the  suffering 
from  breathlessness  and  pain  is  often  very  distressing,  such  as  in  cardio- 
sclerosis with  cardiac  asthma,  Cheyne-Stokes  respiration,  and  angina  pectoris. 
In  these  cases  I  reasoned  that  the  exhaustion  of  the  heart  muscle  that 
induced  these  distressing  symptoms  was  due  to  deficient  nourishment. 
As,  however,  the  tissues  were  bathed  in  the  lymph  which  contained  the 
salts  necessary  for  the  nourishment  of  the  heart,  it  might  be  the  deficiency 
of  oxygen  that  was  the  main  cause  of  exhaustion.  I  therefore  employed 
HiU's  method  of  giving  concentrated  oxygen,  and  in  the  first  few  cases 
I  met  with  most  gratifying  success  :  patients  who  had  suffered  for  months 
from  restless  and  disturbed  nights  due  to  dyspnoea  and  pain  obtained 
great  and,  in  some  cases,  immediate  relief.  Further  experience,  however, 
showed  that  apparently  similar  cases  in  which  'prima  facie  I  would  have 
expected  the  same  satisfactory  results,  little  or  no  relief  was  obtained. 
The  matter  therefore  requires  further  consideration  in  order  to  recognize 
more  accurately  the  class  of  patient  that  should  benefit  by  oxygen,  and 
I  give  here  a  short  description  of  HiU's  method,  which  I  have  used. 

I  have  found  that  in  attempting  to  give  oxygen  in  a  concentrated  form, 
a  mask  like  a  chloroform  mask  conveys  to  the  patient  a  sense  of  suffocation. 
HiU  employs  a  mask  of  a  very  simple  kind.  A  piece  of  light  macintosh 
cloth  about  two  feet  square  is  taken,  and  near  one  side  a  hole  is  cut  in  the 
middle  over  which  is  glued  a  piece  of  transparent  celluloid  six  inches  square. 
An  elastic  band  is  attached  around  this  border  of  the  macintosh,  so  narrow 
that  it  will  grasp  the  head  lightly  in  such  a  position  that  the  celluloid  covers 
the  face  while  the  remainder  of  the  macintosh  is  lightly  packed  around  the 
neck.  The  oxygen  direct  from  the  cylinder  is  introduced  by  a  tube  through 
a  hole  below  the  celluloid.  The  cool  cmrent  of  oxygen  is  felt  as  refreshing, 
and  is  greatly  appreciated  by  the  patient.  I  generally  give  a  fair  stream 
of  oxygen  for  15-20  minutes — using  in  that  time  10-12  feet  of  oxygen. 

When  this  mask  is  not  available  (it  can  be  had  from  Siebe,  Gorman  &  Co., 
187  Westminster  Bridge  Road,  London)  I  have  employed  a  lady's  hat-box, 
cutting  out  of  the  side  a  space  for  the  patient's  neck,  so  that  the  patient's 
head  goes  comfortably  into  the  box.  I  then  put  on  the  lid,  and  pass  the 
tube  from  the  cylinder  through  a  small  hole  in  the  side  of  the  box. 

This  method  of  giving  the  oxygen  is  rather  wasteful,  and  for  economy 


280  DISEASES  OF    THE   HEART 

another  method  may  be  tried  where  the  oxygen  is  given  by  means  of  a  bag, 
and  the  patient  inspires  and  expires  through  a  tube,  where  by  a  valvular 
arrangement  the  expired  air  passes  through  a  tin  containing  sticks  of  caustic 
soda,  which  takes  up  the  CO^  while  the  oxygen  is  led  back  to  the  bag  to 
be  respired  again.  This  apparatus  is  also  made  according  to  Hill's  design 
by  Siebe,  Gorman  &  Co. 

Leonard  Hill  has  also  devised  a  simple  apparatus  by  which  a  patient 
can  make  a  small  quantity  of  oxygen  and  use  it  as  desired.  It  consists 
of  a  small  metal  box — the  generator — connected  with  a  vulcanized  rubber 
breathing-bag.  The  bag  holds  about  15  litres  of  gas,  and  ends  in  a  mouth- 
piece. The  bottom  of  the  generator  is  formed  by  a  screw-lid  fitted  with 
asbestos  washer.  A  piece  of  wire  gauze  is  interposed  between  the  generator 
and  the  bag.  A  screw-clip  closes  the  mouth-piece  during  the  generation 
of  the  gas.  The  oxygen  is  generated  out  of  oxylithe  (NagOg)  by  contact 
with  water,  and  a  solution  of  caustic  soda  results  which  is  used  to  absorb 
the  exhaled  carbonic  acid.  Na^Og  +  H^O  =  ^^aOH -I- Og.  The  oxylithe  is 
sold  in  flat  tins  containing  ten  blocks  to  the  pound,  and  three  blocks  make 
a  charge  sufficient  for  fifteen  minutes'  inhalation. 

The  bag  is  laid  flat  on  the  table  and  emptied  of  air.  The  oxyUthe  is 
then  put  into  the  generator,  and  water  introduced  into  the  bag  through  the 
mouth-piece.  The  screw-clip  is  then  closed,  and  the  bag  raised.  Some 
of  the  water  then  enters  the  generator,  and  the  bag  becomes  fuU  of  oxygen. 
The  patient  puts  the  mouth-piece  into  his  mouth  and  a  soft  chp  on  his 
nose,  and,  opening  the  screw-clip,  breathes  in  and  out  of  the  bag,  shaking 
the  solution  round  the  bottom  of  the  bag  meanwhile  to  absorb  the  carbonic 
acid  exhaled.  When  about  two-thirds  of  the  bag  of  gas  has  been  used  up, 
the  instrument  is  washed  out  and  hung  up  to  dry. 


CHAPTER   XXXIV 

Treatment  {continued) 

§  249.  The  action  of  digitalis  on  the  human  heart. 

250.  Action  on  dilatation  of  the  heart. 

251.  Action  on  rate  and  on  the  nodal  rhythm. 

252.  Action  on  conductivity  (heart-block). 

253.  Action  on  contractility. 

254.  Action  on  blood- pressure. 

255.  Digitalis  in  practice. 

256.  Other  drugs  of  the  digitalis  group  (strophanthus,  squills,  helleborein). 

§  249.  The  action  of  digitalis  on  the  human  heart — In  inquiring 
into  the  therapeutic  action  of  digitahs,  I  found  that  the  result  of  clinical 
experience  was  that  digitalis  was  undoubtedly  beneficial,  but  that  it  was 
uncertain  in  its  action,  and  that  the  various  preparations  varied  much 
in  their  potency.  A  wide  divergence  of  opinion  existed  in  regard  to  what 
cases  were  suitable  for  its  administration. 

On  starting  this  inquiry  I  was  at  first  lost  in  confusion,  unable  to  find 
any  sure  line  to  follow.  I  systematically  gathered  a  great  number  of  cases 
where  I  had  given  digitalis,  and,  on  classifying  the  results  obtained,  certain 
clear  issues  came  out,  which  gave  very  definite  lines  for  me  to  follow  in 
the  subsequent  investigation.  A  summary  of  these  results  I  give  here, 
dealing  somewhat  fully  with  a  few  illustrative  cases  in  Appendix  VI. 

In  regard  to  the  question  of  preparation,  I  limited  myself  to  three  different 
forms — viz.  B.P.  Tincture  of  Digitalis,  Nativelle's  Digitalin  Granules,  and 
the  pills  containing  Digitalis,  Squills,  and  Calomel  (R.  Digitalis  pulv.  gr.  |, 
Scillae  pulv.  gr.  |,  Hyd.  subchlor.  gr.  1).  I  did  not  extend  my  observations 
to  other  forms,  as  it  seemed  better,  with  my  limited  field,  to  get  a  definite 
result  from  these  very  diverse  preparations,  than  to  arrive  at  an  indefinite 
result  with  a  multiplicity  of  preparations.  The  results  of  this  investigation 
showed  that  all  three  forms  were  equally  potent  in  certain  cases  and  equally 
impotent  in  other  cases.  As  a  rule,  when  in  one  patient  a  certain  definite 
reaction  was  obtained  by  one  preparation  it  was  also  obtained  by  the 
exhibition  of  the  others.  I  drew  the  conclusion  that  variability  in  the 
action  of  the  drug  did  not  depend  so  much  on  the  preparation  as  on  the 
nature  of  the  lesion  with  which  the  heart  was  affected. 


282  DISEASES  OF  THE  HEART 

§  250.  Action  on  dilatation  of  the  heart. — ^When  I  came  to  inquire 
into  all  the  symptoms  in  these  cases  where  digitalis  had  a  beneficial  action, 
I  found  them  limited  to  those  in  which  there  was  dilatation  of  the  heart- 
But  it  was  not  equally  effective  in  all  cases  of  dilatation.  In  cases  of 
old-standing  rheumatic  affection  with  dilatation  it  was  generally  very 
effective,  and  in  many  cases  with  no  history  of  rheumatism  ;  while  in 
others  of  similar  origin  and  with  heart  failure,  but  without  dilatation  (e.g. 
mitral  stenosis),  digitalis  had  no  beneficial  effect.  In  fact,  I  failed  to  see  any 
evidences  of  a  good  result  in  any  patient  where  the  heart  was  not  dilated. 

The  good  results  obtained  by  the  use  of  digitalis  are  doubtless  due  to 
the  specific  action  of  the  drug  on  the  function  of  tonicity. 

In  acute  dilatation  of  the  heart,  as  in  febrile  affections,  I  could  never  find 
any  improvement  under  it ;  nor  was  there  much  benefit  in  cases  of  dilatation 
secondary  to  advanced  cardio-sclerosis.  In  a  few  cases  some  shght  improve- 
ment might  take  place,  especially  if  there  was  dropsy — a  slight  increase  in 
the  quantity  of  urine.     But  as  a  rule  no  appreciable  benefit  resulted. 

§  251.    Action    on  rate   and    on    the  nodal   rhythm ^When  the 

rhythm  was  normal,  i.  e.  when  the  ventricular  contractions  followed  the 
auricular,  digitaUs  did  not  often  have  much  effect  beyond  slowing  the  rate 
to  a  slight  extent.  In  a  few  cases  of  dilated  heart  with  frequent  action, 
due  to  old-standing  rheumatic  affection,  the  heart  slowed  under  digitaUs, 
but  it  never  feU  below  the  normal.  In  rapid  hearts  in  febrile  affections 
it  never  had  any  influence,  nor  in  the  quick  heart  of  exhausting  disease, 
as  in  tuberculosis,  the  reason  probably  being  that  a  far  more  powerful 
poison  was  already  in  the  possession  of  the  heart. 

In  cases  of  nodal  rhythm  the  action  of  digitalis  is  sometimes  Httle  short 
of  miraculous.  It  is  really  to  its  action  in  these  cases  that  the  digitahs 
group  of  remedies  owe  their  great  reputation.  I  have  endeavoured  to  find 
out  in  the  literature  of  the  subject  the  nature  of  the  cases  which  have 
led  authors  to  eulogize  digitalis,  but  I  have  found  the  greatest  difficulty. 
Most  writers  deal  in  such  general  terms  that  it  is  evident  they  have  not 
reahzed  the  nature  of  the  heart's  lesion  in  which  they  found  digitaUs 
effective.  Where  particulars  have  been  given,  I  could  infer  with  fair  cer- 
tainty that  the  cases  were  those  of  rheumatic  hearts  with  the  nodal  rhythm. 

In  Figs.  152,  153,  and  154  are  given  tracings  which  show  the  action  very 
typicaUy.  In  Fig.  152  the  heart  is  irregular  in  its  action,  80  beats  per 
minute.  The  jugular  pulse  is  of  the  ventricular  form  (nodal  rhythm), 
and  is  typical  of  the  condition  so  common  in  advanced  rheumatic  hearts. 
The  heart  was  dilated  ;  there  was  a  systolic  and  long  diastolic  murmur  at 
the  apex  (see  shading  under  Fig.  153),  the  urine  was  scanty,  and  there  was 


TREATMENT 


283 


much  dropsy.  The  patient  was  put  upon  the  digitalis,  squills,  and  calomel 
pill  three  times  a  day.  In  ten  days'  time  the  heart  became  much  slower, 
and  took  on  the  rhythm  shown  in  Figs.  153  and  154,    The  curious  doubling 


J  ^  i    UJ    1       i  £      / 

lAA^XAiLM M  An 

Fig.  152.  Tracings  from  an  old  rheumatic  case  witli  the  nodal  rhythm,  showing  the  charac- 
teristic irregularity  and  ventricular  venous  pulse.  At  the  post-mortem  examination  there  was 
both  mitral  and  tricuspid  stenosis.  Before  digitalis.  (Figs.  153  and  154  are  from  the  same 
patient.) 


Fig.  153.  Shows  the  characteristic  effect  of  digitalis  in  old  rheumatic  hearts  with  the  nodal 
rhythm.  The  figures  1,  2,  represent  the  first  and  second  sounds  of  the  heart,  and  the  shading 
represents  the  murmurs  present. 


Fig,  154.    Shows  a  digitaUs  effect  with  coupled  beats  and  slow  single  beats, 

of  the  beat  shown  in  these  tracings  is  a  very  common  result  of  digitaHs  in 
this  class  of  case.  With  the  slowing  of  the  pulse  the  patient's  condition 
improved  ;  the  urine  became  more  abundant,  and  the  dropsy  to  a  great 
extent  disappeared. 


284 


DISEASES  OF  THE  HEART 


The  curious  coupling  of  the  beats  in  Fig.  153  requires  consideration  as 
a  matter  of  practical  importance  and  scientific  interest.  If  cases  were 
judged  by  the  pulse  alone  the  nature  of  the  change  would  be  entirely  lost. 


Fig.  155.  Tracings  of  the  radial  and  liver  pulses  before  administration  of  digitalis  from 
an  old  rheumatic  heart,  with  great  dilatation,  and  where  the  mitral  valves  were  shrunken  at 
the  post-mortem  examination.  Figs.  153  and  154  were  taken  from  the  patient  after  the 
administration  of  digitalis. 

Thus,  Fig.  155  is  from  a  patient  with  great  dilatation  of  the  heart  and 
mitral  incompetence — the  valves  damaged  by  an  old  rheumatic  affection 
of  the  heart.     Under  digitalis  the  heart  became   slow,   the  radial  pulse 


Fig.  156.     Tracing  of  the  radial  pulse  (28  per  m.)  after  digitalis.     The  real  nature  of  the 

slowing  is  shown  in  Fig.  157. 

being  at  the  rate  of  28  per  minute  (Fig.  156).  Tracing  Fig.  157,  taken 
simultaneously  from  the  apex  and  liver,  showed  that  both  ventricles  con- 
tracted together,  the  apex  giving  the  characteristic  cardiogram  of  the  left 


Fig.  157.  Simultaneous  tracings  of  the  liver  pulse  and  apex  beat,  showing  complete 
harmony  in  the  rhythm  of  both  ventricles,  Tlie  sounds  and  murmurs  present  are  diagram- 
ma  tically  represented.    After  digitalis. 

ventricle,  while  the  liver  pulse  was  produced  by  the  right  ventricle.  The 
curious  coupling  of  the  beats  is  shown  here,  and  the  slow  radial  pulse  (Fig.  156) 
is  seen  to  be  due  to  the  fact  that  the  smaller  beats  did  not  reach  the  radial. 


TREATMENT 


285 


The  same  features  are  brought  out  in  the  tracings  from  another  patient. 
Fig.  158  shows  the  jugular  and  radial  pulses  when  the  patient  was  not 
under  the  influence  of  digitalis.     Figs.  159  and  160  show  the  action  of  the 


Fig.  158.  Simultaneous  tracings  of  the  jugular  and  radial  pulses.  The  jugular  pulse  is  of 
the  ventricular  type,  and  the  tracing  shows  complete  agreement  in  rhythm  between  the  right 
and  left  ventricles.  From  an  old  rheumatic  heart,  in  which,  at  the  post-mortem  examination, 
there  was  found  great  stenosis  of  the  mitral  orifice.  Before  digitalis.  Figs.  159  and  160  are 
from  the  same  patient. 

heart  due  to  digitaUs,  In  these  tracings,  the  one  of  the  apex  and  radial  and 
the  other  of  the  liver  and  radial,  the  characteristic  coupling  of  the  beats  seen 
in  the  apex  and  liver  is  not  observed  in  the  radial  because  the  smaller 


Fig.  159.  Simultaneous  tracings  of  the  apex  beat  and  of  the  radial  pulse  from  a  case  of 
mitral  stenosis.  The  coupled  beats  are  well  marked  in  the  apex  tracing.  The  shading  under- 
neath shows  the  time  of  the  murmurs.     After  digitalis. 

beats  did  not  affect  the  radial  pulse.  In  this  case  there  was  a  long  diastoUc 
murmur,  as  shown  by  the  shading,  and  the  post-mortem  examination  showed 
extreme  stenosis  of  the  mitral  orifice. 


Fig.  160.     The  coupled  beats  are  well  marked  in  the  liver 
tracing.     After  digitalis. 

I  have  a  large  collection  of  tracings  showing  the  same  results,  and  every 
one  of  them  came  from  patients  with  the  nodal  rhythm,  and  with  a  past 
history  of  rheumatism.  The  practical  importance  of  this  reaction  lies  in  the 
fact  that  the  appearance  of  these  coupled  beats  is  at  once  the  signal  to  lessen 


286  DISEASES  OF  THE  HEART 

the  dose  of  digitalis.  No  good  is  to  be  obtained  by  pushing  it  further, 
and  when  one  can  just  manage  to  keep  the  patient  at  the  stage  where 
this  tendency  occurs  the  best  results  from  digitaUs  will  be  obtained — the 
patient  feels  easier,  makes  more  urine,  and  the  dropsy  is  kept  under 
control. 

The  scientific  interest  lies  in  the  fact  that  no  other  form  of  heart  ailment 
produces  this  reaction.  It  has  never  been  produced  experimentally,  and 
cannot  occur  while  the  auricles  are  active  and  occupying  their  normal 
place  in  the  cardiac  cycle  ;  in  other  words,  it  is  a  reaction  limited  to  patients 
with  the  nodal  rhythm.  I  have  thought  much  on  the  nature  of  this  rhythm, 
but  my  conclusions  are  of  too  speculative  a  nature  to  be  of  any  real  value. 
I  wish,  however,  to  point  out  that  the  second  of  the  linked  beats  are  not 
extra-systoles.  In  §  141  I  defined  an  extra-systole  as  the  premature  occur- 
rence of  an  auricular  or  ventricular  systole  while  the  fundamental  or  sinus 
rhythm  of  the  heart  was  maintained — the  retention  of  that  rhythm 
accounting  for  the  character  of  the  irregularity.  Here  there  is  no  sinus  or 
fundamental  rhythm,  and  as  a  consequence  the  pauses  between  the  beats 
are  continuously  liable  to  variation. 

In  cases  with  the  auricles  active,  the  production  of  extra-systoles  by 
digitalis  does  occur  in  a  small  proportion  of  cases,  but  usually  only  after 
the  drug  has  been  pushed  rather  far.  In  Case  25,  Appendix  VI,  this 
coupling  of  the  beats  occurred  while  the  patient  had  the  nodal  rhythm. 
After  a  time  the  normal  rhythm  was  restored,  and  when  digitalis  was 
pushed  extra-systoles  occurred,  but  the  whole  character  of  the  heart's 
action  was  very  different,  as  a  study  of  the  tracings  given  from  this  case 
wiU  show.  This  coupUng  of  the  beats  has  been  noticed  by  other  observers. 
Thus  Broadbent  ^  describes  the  coupled  beats  as  a  result  of  digitalis,  but  he 
and  others  have  failed  to  appreciate  the  class  of  case  in  which  it  occurred, 
and  did  not  reaUze  it  was  a  reaction  peculiar  to  this  kind  of  heart. 

The  manner  in  which  the  heart-rate  can  be  played  upon  by  digitalis  in 
these  cases  of  nodal  rhythm  is  very  remarkable.  I  have  frequently  seen  the 
heart  increase  in  frequency,  sometimes  very  greatly  (up  to  120-130  beats 
per  minute)  when  the  digitalis  was  withheld,  and  in  the  course  of  a  few 
days  digitalis  often  soon  slowed  it  down  to  between  60  and  70  beats  per 
minute.     (See  Case  25,  Appendix  VI.) 

But  the  effect  is  not  only  upon  the  rate  of  the  heart  :  the  size  of  the 
heart  diminishes,  the  urine  increases,  and  the  dropsy  disappears.  If  there 
be  much  liver  enlargement,  the  digitalis  at  the  same  time  diminishes  the 
size.  Fig.  66,  p.  127,  was  taken  from  a  pulsating  liver  at  the  level  of  the 
umbilicus.     The  patient  was  at  the  time  extremely  breathless,  and  had  to 


TREATMENT  287  . 

be  propped  up  in  bed.  Tincture  digitalis,  15  Q)  three  times  a  day,  was 
prescribed,  and  in  three  days'  time  he  was  up  and  about,  and  no  sign  of 
the  liver  could  be  detected  below  the  ribs. 

I  am  convinced  that  it  is  the  striking  effect  of  digitaUs  in  these  cases 
that  has  led  cUnicians  to  form  such  a  high  opinion  of  this  drug.  FaiUng 
to  recognize  that  the  action  depended  on  the  nature  of  the  lesion,  they  have 
sought  to  find  a  similar  benefit  in  cases  not  so  susceptible  to  it,  and  from 
this  have  arisen  the  confusion  and  contradictory  statements  in  regard  to. 
the  action  of  digitalis. 

No  such  reaction  as  that  shown  in  Figs.  152-160  can  be  obtained,  unless 
where  the  nodal  rhythm  is  present.  And  even  amongst  cases  of  nodal 
rhythm  a  further  differentiation  has  to  be  made,  for  I  never  get  this  result 
in  cases  of  nodal  rhythm  secondary  to  cardio-sclerosis  associated  with 
arterial  degeneration.  In  these  cases  I  have  sometimes  seen  a  little  im- 
provement— an  increase  in  the  flow  of  urine  and  a  diminution  of  the  dropsy, 
and  it  may  be  a  slight  slowing  of  the  heart's  rate — but  never  anything 
approaching  the  slowing  in  old  rheumatic  cases.  In  many  cases,  though 
I  have  pushed  the  drug  till  the  patient  was  sick  and  had  diarrhoea,  I  have 
seen  no  alteration  in  the  heart's  condition.  This  difference  is  probably  due 
to  the  greater  extent  of  the  degeneration  of  the  heart  muscle. 

§  252.  Action  on  conductivity  (heart-block) — In  a  great  many 
cases  I  have  been  able  to  produce  a  mild  form  of  heart-block  by  the  adminis- 
tration of  digitaHs,  and  I  can  now  recognize  the  class  of  case  in  which  this 
occurs.  I  have  already  pointed  out  that  the  interval  between  the  auricular 
systole  and  the  ventricular  can  be  determined  by  the  length  of  the  a-c 
interval  in  tracings  from  the  jugular  pulse  (§  163).  If  this  interval  be 
above  one-fifth  of  a  second  (unless  in  a  very  slow  heart)  it  is  due  to  a  depres- 
sion of  the  function  of  conductivity  of  the  a. -v.  bundle.  When  the  heart's 
action  is  over  100,  with  the  interval  one-fifth  of  a  second,  a  depression  of 
conductivity  may  be  suspected.  By  the  administration  of  digitaHs  in 
a  great  number  of  my  patients  I  have  been  able  to  increase  this  depression 
of  conductivity,  so  that  ventricular  systoles  have  dropped  out  because  the 
stimulus  from  the  auricle  did  not  reach  the  ventricle. 

In  Fig.  161  there  is  a  wide  a-c  interval  (two-fifths  of  a  second).  I  gave 
the  patient  from  whom  this  tracing  was  taken  three  drachms  of  tincture 
of  digitalis  in  the  course  of  four  days,  and  her  pulse  became  irregular,  due  to 
the  dropping  out  of  ventricular  systoles  (Fig.  162).  Some  years  previously 
I  had  produced  a  similar  effect  in  this  patient  by  digitaHs,  when  every 
second  ventricular  systole  dropped  out  (Fig.  163). 

When  digitalis  is  prescribed  for  a  patient  with  a  regular  pulse  and  the 


288 


DISEASES  OF  THE  HEART 


heart  becomes  irregular,  it  is  probably  due  to  this  cause.  The  nature  of 
the  irregularity  can  be  inferred  with  fair  certainty  by  auscultation  when 
the  heart  sounds  are  found  to  be  absent  during  the  pause.  Extra-systoles 
sometimes  follow  the  administration  of  digitalis,  and  the  irregularity  of  the 
pulse  may  resemble  the  dropping  out  of  beats  due  to  heart-block,  but  with 


Ro^d'\a\ 


Fig.  161.  The  a-c  interval  is  twice  the  normal  period  (two-fifths  of  a  second  in  place  of 
one-fifth),  indicating  a  delay  in  the  stimulus  passing  from  the  auricle  to  the  ventricle.  (This 
and  the  next  two  tracings  are  from  a  female,  aged  24  years,  suffering  from  mitral  stenosis.) 

extra-systoles  the  short,  sharp  sounds  of  the  heart  during  the  pause  in  the 
radial  pulse  will  usually  be  detected  (Fig.  87).  In  many  cases  where  there 
is  dilatation  of  the  heart,  as  soon  as  the  irregularity  appears  the  patient 
experiences  a  good  deal  of  relief,  though  sometimes  the  throb  after  the 
pause  is  distressing.     (See  also  Cases  26  and  27,  Appendix  VI.) 


Fig.  162  shows  the  missing  of  a  ventricular  systole  at  frequent  intervals  on  account  of  the 
delay  in  the  stimulus  passing  from  the  auricle.  It  will  be  noticed  that  the  wave  a  is  perfectly 
regular  in  its  appearance,  and  that  its  relationship  to  the  carotid  and  radial  is  variable 
(digitalis  effect).  Note  the  gradual  increase  of  the  size  of  the  auricular  wave,  a,  before  the 
intermission.  Tliis  is  due  to  the  gradual  increase  in  the  width  of  the  a-c  interval  until  the 
auricular  contraction  occurs  before  the  preceding  ventricular  systole  is  completed  (see  also 
Fig.  114). 

In  most  of  the  cases  in  which  I  have  been  able  to  produce  this  condition 
of  mild  heart-block  there  has  been  a  previous  history  of  rheumatic  fever. 

§  253.  Action  on  contractility If  tracings  be  taken  systematically 

of  patients  under  the  influence  of  digitalis,  evidence  of  a  depression  of 
contractility   may   occasionally   be   detected   in   the   form    of   the   pulsus 


TREATMENT 


289 


alternans.     It  is  generally  so  slight  as  to  escape  detection  unless  a  tracing 
be  taken. 

In  Figs.  164  and  166  are  tracings  of  the  pulsus  alternans,  due  in  the  one 


Fig.  163.  Slowing  of  the  pulse  due  to  digitalis  depressing  the  conductivity,  so  that  the 
ventricle  responds  only  to  every  second  stimulus.  Wliile  the  ventricle  contracted  forty-eight 
times  per  minute  the  auricle  contracted  ninety-six  times. 

case  to  digitalis,  squiU,  and  calomel  piU,  and  in  the  other  to  the  tincture 
of  digitalis.  Curiously  enough,  the  appearance  of  this  change  in  the  rhythm 
of  the  pulse  was  accompanied  by  an  improvement  in  the  patient's  con- 


FiG.  164.'    Typical  pulsus  alternans  due  to  digitalis.     (Case  9,  Appendix  11.) 

dition.  The  reason  for  the  improved  condition  when  the  conductivity  of 
the  a.-v.  bundle  and  the  contractihty  of  the  heart  muscle  was  depressed, 
is  in  all  probabihty  a  coincident  improvement  in  the  tonicity.     This  view 


Fig.  165.     Taken  at  the  same  visit  as  164,  and  from  the  same  patient,  to  show  that  the 
conductivity  was  not  affected — the  a-c  interval  being  normal  (one-fifth  of  a  second). 

is  confirmed  by  some  observations  Gossage  has  shown  me.  That  the  function 
of  conductivity  was  unaffected  in  these  two  cases  is  shown  by  the  normal 
a-c  interval  in  the  jugular  tracings  (Figs.  165  and  167). 

§  254.  Action  on  blood-pressure — Contrary  to  expectation,  I  found 
that  it  is  only  in  exceptional  cases  that  the  administration  of  digitalis 


Mackenzie: 


U 


290 


DISEASES  OF  THE  HEART 


raises  the  blood-pressure.  I  have  repeatedly  pushed  it  until  distinct  evidence 
of  its  physiological  action  was  produced  on  the  stomach  or  on  the  heart, 
without  any  apparent  rise  in  the  blood-pressure.  Even  when  the  patient 
was  greatly  benefited  by  the  drug,  I  have  frequently  seen  httle  or  no  evidence 
of  an  increase  in  the  blood-pressure.  The  only  cases  where  I  did  find 
increase  in  the  blood-pressure  were  in  extreme  dilatation  of  the  heart  with 


mummimmmmmmmmmmmmmmmfmmm^i;si^i^^r^ 


Fig.  166.     Typical  pulsus  alternans  due  to  digitalis. 

considerable  dropsy.     In  these   cases  a  slight  rise   in   the   blood-pressure 
accompanies  the  improved  condition  under  digitalis. 

§  255.  Digitalis  in  practice — In  the  following  summary  of  the  con- 
ditions in  which  digitalis  wiU  be  found  to  act  beneficially  it  may  seem  that 
its  field  of  usefulness  is  far  too  restricted.  While  I  do  not  think  so,  I  wish 
to  insist  upon  the  limitations  of  its  usefulness  for  a  very  important  reason, 


Fig.  167.     Taken  at  the  same  visit  as  166,  and  from  the  same  patient,  to  show 
there  was  no  affection  of  the  conductivity,  the  a-c  interval  being  normal. 

namely,  because  the  reliance  placed  upon  this  drug  has  led  to  the  belief 
that  it  should  be  tried  in  all  forms  of  heart  affection,  with  the  result  that 
valuable  time  which  should  have  been  spent  in  putting  the  heart  under 
favourable  conditions  has  been  wasted. 

The  condition  of  heart  failure  where  it  acts  best  is  where  there  is  dilata- 
tion of  the  heart  with  healthy  muscle-fibres  that  have  been  exhausted  in 
the  endeavour  to  overcome  abnormal  resistance.  This  effect  is  best  seen 
in  old  rheumatic  affections  of  the  heart,  but  it  may  also  be  observed  in 
other  cases  with  a  fair  amount  of  healthy  muscle.     It  is  of  very  little  use 


TREATMENT  291 

when  the  dilatation  of  the  heart  is  due  to  extensive  degeneration  of  the 
muscle-fibres,  as  in  cardio-sclerosis.  In  a  sense  the  degree  of  reaction  gives 
a  measure  of  the  extent  of  the  degeneration — the  greater  the  extent  of  the 
degeneration  the  less  the  reaction.  It  will  be  found  to  be  of  little  value 
when  the  heart  is  already  in  the  grip  of  some  poison,  whether  it  be  the 
specific  organism  of  such  disease  as  rheumatic  fever,  pneumonia,  or  the 
toxins  of  such  diseases,  or  such  poisons  as  alcohol  and  arsenic. 

This  conclusion,  drawn  from  the  careful  study  of  individual  patients,  is 
in  striking  accordance  with  the  conclusions  drawTi  by  Cushny  ^*  from  experi- 
ment :  '  In  cases  of  dilatation  of  the  heart  with  a  weak  and  insufficient 
systole  its  action  is  almost  specific.  This  is  true  whether  one  or  both 
ventricular  chambers  are  affected,  so  long  as  the  cardiac  muscle  has  not 
undergone  degeneration.' 

When  the  heart  becomes  continuously  irregular  (nodal  rhythm)  in  old 
rheumatic  cases,  digitalis  usually  acts  with  great  promptness  and  certainty. 
In  these  cases  the  administration  should  be  kept  up  for  considerable  periods, 
just  sufficient  of  the  drug  being  given  to  keep  the  rate  between  60  and 
70  beats  per  minute,  or  until  the  characteristic  coupled  beats  appear.  Some- 
times good  results  are  obtained  when  the  rate  cannot  be  reduced  so  low. 
Under  such  circumstances  the  condition  of  the  patient  in  other  respects 
should  be  the  guide,  the  dose  being  modified  according  to  the  degree  of 
improvement. 

In  cases  of  nodal  rhythm  due  to  other  conditions  the  heart  is  not  so 
susceptible,  and  great  caution  should  be  exercised  in  the  prescription  of 
digitaHs  here.  Occasionally  we  read  of  precautions  in  the  use  of  digitalis, 
and  of  its  tendency  to  cause  a  fatal  stoppage  of  the  heart,  but  I  have  been 
unable  to  determine  the  form  of  heart  disease  in  which  these  sudden  deaths 
are  liable  to  occur.  The  only  cases  of  sudden  death  I  have  seen  during 
the  administration  of  digitalis  were  unyielding  cases  of  nodal  rhythm.  In 
one  patient  with  cardio-sclerosis  I  was  carefully  pushing  it,  when  the 
patient  died  suddenly  in  the  night.  In  another  case  of  rheumatic  origin, 
digitalis  had  little  effect,  and  the  patient  had  taken  only  an  occasional 
dose  when  she  died  suddenly  while  dressing  one  morning.  But  I  am  not 
clear  in  my  mind  that  the  digitalis  had  any  part  in  the  sudden  end  of  these 
cases,  and  there  was  no  preliminary  slowing  of  the  heart's  action. 

§  256.  Other  drugs  of  the  digitalis  group  (strophanthus,  squills, 
helleborein) — I  have  used  other  drugs  of  this  group  (strophanthus,  squills, 
heUeborein),  but  only  to  a  limited  extent.  So  far  as  my  observations 
extended,  I  found  that  if  digitalis  failed  to  act  they  also  failed.  I  tried 
strophanthus  on  several  cases  that  were  susceptible  to  digitahs  and  got 

U  2 


292  DISEASES  OF  THE  HEART 

the  same  reaction,  but  only  after  a  much  longer  time.  This  result  was  in 
striking  agreement  with  the  experience  of  a  very  intelligent  man  whom 
I  saw  in  consultation.  He  had  had  rheumatic  fever,  and  his  heart  had 
acquired  the  nodal  rhythm.  For  many  years  he  had  been  hable  to  fre- 
quent breakdowns,  but  could  pull  himself  together  with  digitalis,  and 
he  always  knew  the  exact  quantity  to  take.  He  told  me  he  had  tried 
strophanthus,  but  that,  while  it  restored  him,  it  took  a  much  longer  time 
to  do  so  than  digitaHs. 

Some  observers  have  found  that  cases  have  responded  to  strophanthus 
after  digitahs  had  bi^en  tried  and  been  found  ineffective.  We  must  be  on 
our  guard  against  the  conclusion  drawn  from  such  an  observation,  for  it 
is  possible  that  the  digitahs  had  in  a  measure  prepared  the  way  for  the 
strophanthus,  for  it  often  happens  that  no  effect  is  obtained  from  the 
digitahs  until  it  has  been  pushed  for  some  time. 


CHAPTER   XXXV 

Treatment  (continued) 


§  257. 

Venesection. 

258. 

Exercises. 

259. 

Massage. 

260. 

Special  movements  and  exercises. 

261. 

Baths. 

262. 

Spa  treatment. 

263. 

Nauheim  baths. 

264. 

Cause  of  efficacy  of  the  spa  treatment. 

There  are  a  great  number  of  other  methods  that  are  useful  in  relieving 
the  patient  or  in  assisting  in  restoring  the  reserve  force  of  the  heart,  and 
I  deal  here  with  the  most  important  of  them. 

§  257.  Venesection — In  a  number  of  cases  the  abstraction  of  blood 
from  the  patient  affords  very  considerable  relief.  Unfortunately  the  rehef 
is  only  temporary,  and  in  extreme  cases  only  delays  the  end.  Although 
I  have  practised  venesection  in  a  great  variety  of  cases,  I  cannot  say 
I  have  seen  it  do  any  lasting  good.  The  indications  for  its  use  that  have 
been  my  guide  have  been  distress  in  breathing,  on  account  of  great  distension 
of  the  right  heart.  In  cases  of  mitral  disease  this  has  generally  been  recog- 
nized by  the  increase  of  the  heart's  dullness  to  the  right.  In  cases  of  high 
blood-pressure  (cardio-sclerosis)  it  has  sometimes  been  difficult  to  detect 
much  enlargement  of  the  right  heart,  and  the  tense  filHng  of  the  veins  of  the 
arm  has  been  the  indication.  I  have  always  bled  at  the  usual  place — at  the 
bend  of  the  elbow — and  abstracted  from  twenty  to  thirty  ounces  of  blood. 
The  immediate  relief  given  to  the  patient  is  often  very  striking. 

§  258.  Exercises — The  heart,  like  every  other  organ,  becomes  more 
efficient  with  reasonable  exercise  of  its  functions,  while  with  a  too  limited 
exercise  the  store  of  reserve  force  gradually  dwindles,  so  that  most  people 
who  pursue  sedentary  occupations  have  a  Limited  field  of  cardiac  response. 
When  such  people  exhibit  some  cardiac  abnormality,  such  as  an  irregularity, 
a  murmur,  or  a  fainting  attack,  the  easily  exhausted  store  of  reserve  force 
shown  by  the  shortness  of  breath  and  palpitation  on  exertion  is  too  often 
taken   as   an    evidence   of  serious   affection  of   the   heart.     Tliis   is    more 


294  DISEASES  OF  THE  HEART 

particularly  the  case  in  the  young  with  sinus  arrhythmia  (youthful  form 
of  irregularity)  and  in  chlorotic  females.  Improvement  in  all  these  cases  is 
best  obtained  by  the  gradual  increase  in  the  daily  amount  of  bodily  exercise. 
In  the  great  majority  of  cases  of  serious  heart-failure,  even  after  recovery 
has  set  in,  the  judicious  employment  of  muscular  exertion  is  beneficial.  It 
may  be  a  matter  of  difficulty  to  determine  whether  more  serious  cases  are 
fit  for  exertion,  and  if  so  to  what  extent.  There  is  a  very  simple  rule  that 
I  have  been  accustomed  to  follow  for  many  years  with  the  greatest  satis- 
faction :  let  the  patient  employ  that  form  of  muscular  exercise  which  he 
can  best  do  without  cardiac  discomfort,  and  never  indulge  in  it  after  the 
first  sign  of  discomfort.  By  discomfort  I  mean  the  various  signs  which  are 
given  by  the  heart  when  its  reserve  force  is  exhausted — as  breathlessness, 
palpitation,  sense  of  exhaustion,  pain.  Discomfort  may  be  experienced 
first  in  the  muscles  exercised,  when  some  particular  group  of  muscles  is 
more  particularly  employed,  as  certain  thigh  muscles  in  climbing,  and  certain 
arm  muscles  in  plajdng  golf — indications  more  of  want  of  training  of  these 
muscles  than  of  heart  exhaustion.  This  form  of  discomfort  need  not  prevent 
further  exercise. 

If  the  rule,  that  exercise  should  stop  short  of  exhaustion,  be  followed, 
it  is  surprising  what  an  amount  of  effort  can  ultimately  be  endured  by 
patients  who  may  once  have  suffered  from  extreme  heart  failure.  This 
will  be  appreciated  by  those  who  practise  among  the  classes  employed  in 
hard  manual  labour.  They  may  have  continually  irregular  hearts  (nodal 
rhythm),  with  aortic  and  mitral  murmurs,  and  may  have  suffered  at  times 
from  the  most  extreme  failure  of  the  heart  with  extensive  dropsy,  yet  they 
can  undertake  the  most  severe  form  of  manual  labour  with  no  discomfort. 
In  such  cases  the  heart  muscle  is  healthy  and  capable  of  acquiring  a  con- 
siderable store  of  reserve,  and  it  is  from  observing  such  patients  that  I  base 
the  prognosis  of  heart  cases  so  much  on  the  power  of  the  heart  to  regain 
its  reserve  force. 

AVlien  patients  can  go  out,  their  exercise  should  be  in  the  open  air,  even 
though  it  is  limited  to  certain  gymnastic  movements.  If  they  can  walk 
quietly,  that  in  itself  may  be  sufficient,  and  if  the  walk  be  taken  system- 
atically a  great  amount  of  reserve  force  may  ultimately  be  acquired.  As 
a  rule,  people  benefit  more  by  exercise  when  it  has  an  object  beyond  the 
medical  needs.  Hence  the  added  interest  of  a  game  or  the  study  of  objects 
of  interest,  as  architecture,  botany,  &c.,  will  add  materially  to  the  efficiency 
of  the  exercise.  The  particular  taste  of  each  patient  has  therefore  to  be 
studied,  and  the  form  of  exercise  prescribed  that  is  likely  to  combine  the 
therapeutic  with  personal  interest. 


TREATMENT  295 

When  patients  are  confined  to  the  house,  or  to  bed,  moderate 
exercise  of  the  muscles  proves  useful,  so  long  as  it  does  not  embarrass 
the  heart.  To  this  end  the  various  movements  and  gymnastics  may  be 
of  use. 

The  good  results  of  exercise  are  obtained  by  a  variety  of  obscure  pro- 
cesses. The  increased  functional  activity  of  the  heart  assists  in  accelerating 
its  own  circulation  and  in  restoring  its  strength,  but  there  are  also  changes 
in  the  circulation  of  the  muscles  exercised  which  lead  to  a  freer  flow  of  blood 
through  the  system.  The  contraction  of  a  muscle  expels  blood  from  its 
capillaries,  and  is  at  once  followed  by  a  dilatation  of  the  capillaries.  This  is 
well  seen  when  the  hand  and  arm  are  placed  in  a  plethysmograph,  and  the 
variation  in  their  bulk  registered.  After  a  single  closing  of  the  fist,  the  bulk 
of  the  arm  at  once  increases  from  the  dilatation  of  the  capillaries  of  the  used 
muscles. 

§  259.  Massage — A  benefit  similar  to  that  of  exercise  can,  in  a 
measure,  be  attained  by  massage.  It  is  not  necessary  that  a  skilled 
person  should  apply  it,  for  that  would  exclude  its  use  among  the  majority 
of  sufferers.  The  gentle  but  firm  intermittent  pressure  upon  the  muscles 
in  the  body  is  quite  sufficient.  In  dropsical  cases  the  gentle  but  firm 
massage  of  the  legs  may  prevent  the  dropsy  reaching  the  extreme  degree 
where  the  skin  becomes  thin  and  glistening  and  liable  at  any  moment  to 
ulcerate.  In  some  extreme  forms  of  the  condition  I  have  referred  to  as 
the  X  disease,  when  there  is  a  persistent  contraction  of  the  smaller  blood- 
vessels of  the  extremities,  massage  has  been  attended  with  benefit. 

§  260.  Special  movements  and  exercises There   is   a  number   of 

methods  employed  involving  muscular  exercises  that  have  gained  con- 
siderable repute.  Such  methods  may  have  a  limited  usefulness  when 
patients  cannot  take  natural  exercise.  Their  chief  recommendation  seems 
to  be  in  reheving  the  tedium  of  convalescence,  and  in  giving  mental 
satisfaction  to  the  patient  that  something  is  being  done.  I  have  made 
a  careful  inquiry  into  the  effects  of  passive  resistance  movements  and 
voluntary  contractions  of  the  muscles,  and  could  find  no  appreciable  effect 
upon  the  heart.  In  certain  people,  especially  those  of  a  slightly  neurotic 
habit,  the  slowing  of  the  pulse  at  the  end  of  the  seance  was  sometimes 
very  marked,  but  I  found  I  could  produce  exactly  the  same  result  by 
employing,  with  equal  solemnity,  indifferent  acts,  such  as  stroking  the 
finger  nails  and  the  shin  bones.  No  effect  was  produced  on  hearts  acting 
at  a  frequent  rate  in  consequence  of  serious  heart  failure  or  the  nodal 
rhythm.  On  no  occasion  could  I  detect  any  decrease  in  the  size  of  the 
heart  as  a  result  of  the  movements.     That  certain  hearts  may  become 


296  DISEASES  OF  THE  HEART 

slow  and  diminish  in  size  after  a  month's  restful  treatment  every  one  will 
acknowledge,  but  it  is  assuming  too  much  to  say  that  such  results  were 
due  to  the  special  method  employed. 

§  261.  Baths. — A  very  powerful  influence  can  be  exercised  on  the 
circulation  by  the  immersion  of  the  body  in  water  ;  this  may  act  in  several 
ways,  perhaps  mainly  depending  on  the  temperature.  Great  thera- 
peutic efficacy  is  claimed  for  certain  waters,  but  it  is  very  doubtful  if  the 
ingredients  in  these  waters  have  any  effect  upon  the  heart,  beyond  their 
effect  in  stimulating  the  skin.  My  personal  experience  has  been  limited 
to  observing  the  results  in  patients  who  have  returned  from  the  various 
spas,  and  I  have  seen  nothing  of  their  good  effects  to  lead  me  to  place 
hydrotherapy  very  high  as  a  means  of  treating  affections  of  the  heart.  The 
best  results  I  have  seen  have  been  in  patients  who  have  bathed  in  the  open 
sea.  When  I  have  had  patients  with  heart  trouble  who  were  fond  of  sea- 
bathing, I  have  allowed  them  to  indulge  in  it,  warning  them  to  be  honest 
with  themselves,  and  refrain  if  it  brought  on  any  sense  of  discomfort.  In 
many  cases  the  result  has  been  extremely  satisfactory,  the  whole  system  of 
the  patients  has  been  braced  up,  and  they  have  returned  from  the  hoHday 
greatly  benefited. 

§  262.  Spa  treatment — Sea-bathing  has,  after  all,  only  a  limited 
sphere  of  usefulness,  and  many  patients  obtain  great  benefits  from  visiting 
spas,  and  the  supporters  of  each  claim  for  its  waters  some  special  virtue. 
In  order  to  assess  the  value  of  these  claims,  it  is  well  to  bear  in  mind  by 
what  process  benefit  is  obtained  at  the  various  spas.  The  vast  majority  of 
patients  go  there  as  much  for  a  hohday  as  for  treatment,  and  when  a  patient 
is  sent  there,  it  is  often  because  the  individual,  in  addition  to  his  complaint, 
has  been  busy  with  his  affairs,  and  his  heart  complaint  has  been  thereby 
aggravated  ;  or  a  patient  is  convalescent,  and  a  change  of  air,  scene,  and 
mode  of  fife  is  often  found  beneficial.  As  the  various  spas  cater  for  the  more 
enjoyable  side  of  existence,  they  attract  large  numbers  of  invahds  who 
naturally  desire  the  reputed  benefits  of  the  waters,  and  drink  them  enthu- 
siastically, or,  if  they  cannot  drink  them,  at  the  least  bathe  in  them. 
It  will  thus  be  seen  that  the  benefits  gained  at  such  places  arise  from 
a  variety  of  sources,  and  it  is  but  human  nature  to  attribute  what  benefit 
has  accrued  to  the  factors  that  most  appeal  to  the  imagination,  such  as 
hot  gaseous  waters  from  the  bowels  of  the  earth.  Every  practitioner  of 
experience  wiU  agree  with  me  that  a  large  proportion  of  heart  cases  return 
from  their  holiday  greatly  improved,  and  this  improvement  is  not  limited 
to  those  who  went  to  some  particular  spa,  but  includes  aU  sorts  of  places — 
spas,  seaside  and  mountain  resorts,  sailing  on  sea  and  lake.     It  is  evident 


TREATMENT  297 

that  results  thus  obtained  cannot  be  due  to  the  peculiar  constituents  or 
the  waters  of  any  single  place. 

§  263.  The  Nauheim  baths — When  I  began  to  write  this  book  the 
purpose  was  to  give  a  faithful  account  of  my  own  experience.  It  was  no 
part  of  my  project  to  enter  into  controversial  matters,  and  in  matters  of 
dispute  I  have  simply  expressed  my  own  views.  But  I  feel  it  would  be 
misleading  if  I  passed  in  silence  a  method  of  treatment  that  has  obtained 
s,  world-wide  reputation  which  I  consider  out  of  proportion  to  its  merits. 
Though  I  enter  into  this  matter  reluctantly,  I  conceive  it  none  the  less  a  duty 
to  give  my  views  on  it,  particularly  as  I  am  impressed  with  the  injury  done 
to  individual  patients  through  the  unmerited  reputation  of  the  Nauheim 
baths  among  the  medical  profession.  Institutes  have  been  started  for  the 
financial  exploitation  of  the  Nauheim  waters,  and  I  must  confess  to  a  feeling 
of  shame  for  my  profession,  when  I  consider  the  manner  in  which  it  has  been 
imposed  upon.  One  reads  in  sober  Enghsh  medical  journals  accounts  of 
cures  effected  that  seem  like  the  puffs  of  an  empiric  remedy.  One  writer 
will  teU  how  a  patient  obtained  no  benefit  from  his  treatment,  but  was  cured 
by  a  visit  to  Nauheim.  Another  describes  how  he  watched  the  patients 
enter  into  the  bath-room  feeble,  tottering,  and  Hvid,  and  how  they  came 
out  upright  and  brisk,  with  a  glow  of  health  on  their  countenances.  It  is 
little  wonder  that  the  stay-at-home  practitioner  is  impressed  by  all  this 
dithyrambic  praise.  The  following  painful  experience  resulted  directly 
from  this  indiscriminate  exaltation  of  the  virtues  of  the  Nauheim  waters. 
I  saw  a  man  in  consultation  whose  history  was  this  :  He  was  seized 
with  symptoms  of  heart  failure,  and  not  improving  as  he  liked,  his 
doctor  advised  him  to  go  to  Nauheim.  An  eminent  physician  was  con- 
sulted later  who  also  strongly  recommended  Nauheim.  Visiting  another 
part  of  the  country,  he  was  taken  iU,  and  the  doctor  who  saw  him  there 
also  told  him  to  go  to  Nauheim.  He  was  so  impressed  with  the  advice  given 
independently  by  three  doctors,  that  he  made  up  his  mind  to  follow  it  and  go 
to  Nauheim.  His  circumstances  were  such  that  he  had  to  stop  all  his  pro- 
fessional work  and  to  expend  a  sum  of  money  that  he  could  ill  afford.  He 
was  only  able  to  travel  to  Nauheim  by  easy  stages,  and  took  three  days  on 
the  journey,  arriving  there  spent  and  exhausted.  He  was  put  through  the 
routine  treatment  of  the  baths,  and  had  digitahs  prescribed  in  addition. 
He  returned  to  England  worse  than  when  he  set  out,  though  bearing  with 
him  a  letter  from  the  Nauheim  physician  saying  that  he  had  greatly  improved 
by  his  visit.  The  patient  himself  shrewdly  remarked  that,  seeing  that 
he  arrived  there  dead  beat  from  his  journey,  it  would  have  been  surprising 
if  he  had  not  picked  up  a  httle  by  the  rest,  but  as  to  his  condition  he  had 


298  DISEASES  OF  THE  HEART 

gained  no  benefit,  but  the  reverse,  from  his  trip.  When  I  saw  him  after  his 
return,  his  was  an  undoubted  case  of  advanced  cardio-sclerosis,  with  extreme 
exhaustion  of  the  heart  muscle.  The  organic  changes  were  irremediable, 
but  the  exertion  of  going  to  and  from  Nauheim  had  injuriously  exhausted 
the  heart,  and  no  doubt  hastened  the  end  of  the  patient,  in  addition  to 
exhausting  his  financial  resources,  for  which  those  dependent  on  him  had 
to  suffer. 

This  is  b}'  no  means  an  exceptional  instance,  and  one  physician  of 
experience  tells  me  that  every  year  he  is  called  upon  to  treat  a  number  of 
the  '  Nauheim  wrecks  ',  as  he  calls  them,  on  their  return.  But  I  do  not  wish 
to  seem  to  condemn  a  method  without  reason,  and  shall  briefly  recount  my 
experiences  in  an  attempt  to  appreciate  the  curative  virtues  of  the  Nauheim 
methods. 

On  arriving  at  Nauheim  and  interviewing  several  doctors  as  to  how  the 
efficacy  of  the  cure  was  to  be  investigated,  I  discovered  that  in  serious  cases 
no  practising  physician  believed  the  waters  to  possess  sufficient  curative 
properties,  but  that  accessory  means  had  to  be  taken  if  a  good  result  was 
to  be  obtained.  Nor  could  I  find  among  those  practising  there  any  agree- 
ment in  regard  to  what  was  the  best  accessory  means.  One  said  the  waters 
were  good  when  assisted  by  the  additional  movements  attained  by  the 
machinery  of  the  Zander  Institute  ;  another  derided  the  use  of  the  Zander 
machinery,  and  said  the  best  effects  were  obtained  from  the  baths  combined 
with  his  specially  invented  method  of  exercise  ;  while  a  third  said  the  methods 
of  the  other  two  were  of  little  avail,  and  that  the  best  results  were  obtained 
when  to  the  baths  something  extra  was  added — such  as  an  electric  current. 
When  all  these  methods  and  baths  were  of  little  avail,  every  doctor  prescribed 
in  addition  drugs  of  the  digitalis  group.  It  was  hopeless  for  me  to  attempt 
to  find  out  the  efficacy  of  any  given  bath  or  method  when  such  complications 
were  introduced,  so  I  did  what  httle  I  could  to  understand  the  influence  of 
the  baths. 

I  found  that  ten  to  twenty  years  ago,  when  the  notion  was  prevalent 
that  to  have  a  good  heart  you  must  have  a  strong  pulse,  these  baths  had 
a  remarkable  effect  in  strengthening  the  pulse,  raising  the  arterial  pressure 
20,  30,  and  40  mm.  Hg.  But  now^adays  the  fashion  being  to  soften  a  strong 
pulse,  these  waters  are  discovered  to  have  a  remarkable  effect  in  lowering 
the  arterial  pressure.  So  remarkable  are  these  waters  that  it  is  claimed 
that  they  can  increase  the  pressure  when  it  is  low,  and  lower  the  pressure 
when  it  is  high. 

I  found  that  these  baths  were  so  modified  as  to  be  of  different  strengths, 
and  it  was  stated  that  the  different  baths  were  given  according  to  the  nature 


TREATMENT  299 

of  the  complaint.  But  I  could  find  no  evidence  of  any  rule  being  followed. 
I  found  that  people  with  nothing  the  matter  with  their  hearts  were  having 
the  same  baths  as  those  who  were  suffering  from  severe  heart  affection. 
I  also  found  patients  with  a  weak  frequent  pulse  having  the  same  baths  as 
others  with  a  slow  hard  pulse. 

I  saw  nothing  which,  by  the  greatest  stretch  of  imagination,  could  confirm 
the  statement  that  patients  are  to  be  seen  entering  these  baths  bent  and  ill 
and  coming  out  of  them  straight  and  strong.  In  the  patients  I  watched  in 
the  baths,  I  could  discover  no  improvement  from  the  single  immersion. 
Certain  effects  on  the  heart,  such  as  slowing  of  its  action,  did  occur  in  several 
cases,  notably  in  healthy  hearts,  as  in  my  own  case  and  in  that  of  a  friend 
whom  I  watched.  This  was  in  the  strong  sprudel  bath,  when  the  tem- 
perature of  the  water  was  89°  F.  But  it  seemed  to  me  merely  a  temperature 
effect,  and  this  was  confirmed  by  the  fact  that  when  I  returned  home  I  found 
my  pulse-rate  and  that  of  my  friend  slowed  in  exactly  the  same  manner 
when  we  lay  in  a  bath  of  ordinary  tap-water  at  the  same  temperature. 
I  found  this  experience  corroborated  in  a  series  of  careful  observations  by 
Reissner  and  Grote,  who  compared  the  effects  of  the  waters  from  these 
springs  with  those  of  plain  water  at  the  same  temperature,  and  found  the 
slowing  of  the  heart  entirely  dependent  on  the  temperature.  This  effect 
of  temperature  is  practically  never  referred  to,  but  is  attributed  to  some 
specific  effect  of  the  waters  on  the  skin.  Thus  in  lying  in  the  bath,  the  water 
being  charged  with  carbonic  acid,  this  gas  comes  off  in  innumerable  small 
bubbles  which  can  be  seen  adhering  to  the  skin.  At  the  same  time  the  skin 
becomes  red.  These  very  simple  phenomena  are  pointed  out  as  in  some  way 
bringing  about  a  reflex  stimulation  of  the  heart. 

§  264.  Cause  of  the  efficacy  of  the  spa  treatment — It  may  be 
said,  and  truthfully,  that  large  numbers  of  people  flock  to  Nauheim 
and  many  of  them  derive  great  benefit  from  the  treatment.  I  recognize 
this,  and  have  carefully  endeavoured  to  find  out  the  reason  for  the  success 
of  the  Nauheim  methods.  When  the  cases  that  are  cured  and  the  cause  of 
then-  cure  are  strictly  analysed,  it  will  be  found  that  at  Nauheim  what  I  call 
the  essentials  of  treatment  are  carried  out  in  an  excellent  manner.  Every- 
thing is  conducive  to  the  restfulness  of  the  patient.  It  is  a  pleasant  place, 
sunny  and  weU  shaded,  with  beautiful  gardens  and  an  excellent  band. 
People  jaded  with  their  cares  and  duties  find  here  that  repose  which  is 
essential  to  the  recovery  of  the  heart.  A  very  large  proportion  of  them 
are  somewhat  neurotic,  and  there  is  consequently  a  very  susceptible 
mental  element  that  can  be  influenced.  The  patient  comes  to  Nauheim 
buoyed  up  mth  the  reputation  of  the  place.     When  he  consults  a  doctor, 


300  DISEASES  OF  THE  HEART 

he  is  confidently  told  that  the  treatment  will  do  him  good — at  once  half 
the  cm'e  is  effected  in  a  great  proportion  of  the  cases. 

Of  wonderful  cm:es  I  saw  none.  Pursuing  my  work  in  a  remote  manu- 
facturing town,  when  I  read  of  the  wonderful  cures  performed  at  places  like 
Nauheim,  I  imagined  that  these  would  be  the  class  of  cases  that  I  failed 
to  benefit.  What  was  my  surprise  to  find  at  Nauheim  that  the  so-called 
wonderful  cures  that  were  being  effected  were  identical  with  those  that 
practitioners  achieve  at  home. 

I  found  at  Nauheim  that  which  I  had  also  found  at  other  spas,  that  the 
practitioners  there  were  scarcely  aware  of  what  the  human  heart  was  capable. 
Those  who,  like  myseff,  have  practised  largely  among  the  better  working 
class  know  what  enormous  capacity  for  recovery  it  possesses.  Many  of  the 
ailments  I  saw  at  Nauheim  would  not  keep  a  working  man  or  woman  from 
their  work,  and  here  they  were  going  through  elaborate  methods  of  cure. 
I  may  frankly  confess  that  I  saw  no  patient  get  benefit  at  Nauheim  who 
would  not  have  done  equally  well  elsewhere. 

The  argument  is  used  that  cases  that  have  been  treated  elsewhere  without 
success  have  obtained  benefit  at  Nauheim.  What  doctor  of  experience  has 
not  the  same  to  tell  ?  I  have  repeatedly  had  patients  place  themselves 
under  my  care  who  had  been  treated  by  other  doctors,  and  they  have  bene- 
fited. But  I  trust  I  am  not  so  foolish  as  to  fancy  the  recovery  was  due  to 
my  skill.  In  many  heart  cases  the  early  stages  of  recovery  are  very  pro- 
tracted, and  marked  improvement  often  takes  place  with  some  shght  change 
in  the  treatment,  and  the  conclusion  is  often  too  hastily  drawn  that  the 
recent  change  effected  the  cure,  whereas  the  heart's  power  was  being  slowly 
restored  by  the  treatment  previously  employed. 

I  have  gone  into  the  subject  of  the  Nauheim  treatment  at  length,  so  that 
the  reader  may  appreciate  the  strength  or  weakness  of  the  position  I  take 
up,  and  I  want  each  practitioner  seriously  to  consider  his  responsibihty  in 
every  case  before  recommending  an  elaborate  and  expensive  treatment.  If 
the  individual  is  well  to  do,  and  there  is  not  much  the  matter  with  him — weU, 
Nauheim  is  as  good  a  place  to  send  him  to  as  any  other.  But  when  it  means 
crippHng  a  man's  resources  either  by  the  outlay  or  by  stopping  his  work, 
a  grave  responsibility  rests  upon  his  adviser. 

In  the  case  of  growing  boys  and  girls,  I  think  Nauheim  and  the  various 
methods  are  distinctly  detrimental  when  the  heart's  weakness  is  purely 
functional  and  the  symptoms  consist  in  occasional  fainting  and  some 
enlargement  and  irregularity  of  the  heart.  This  class  of  patient  is  often 
sent  there,  and,  in  consequence  of  the  elaborate  ritual,  they  get  the  notion 
there  must  be  something  serious,  and  go  through  Ufe  under  the  impression 


TREATMENT  301 

that  they  have  a  weak  heart,  with  the  consequences  seen  in  the  malade 
imaginaire.  I  have  seen  numbers  of  these  going  through  these  elaborate 
methods  whom  I  would  have  sent  out  to  the  play-fields. 

The  assembling  in  crowds  of  neurotic  people  is  a  bad  feature. 
They  are  so  fond  of  detailing  their  symptoms  to  one  another  that  they 
cultivate  the  habit  of  self -analysis.  If  this  were  done  sanely,  good  might 
result,  but  it  often  ends  in  making  the  individual  too  self-conscious  of 
what  little  infirmity  he  suffers  from,  so  that  I  prefer  to  send  my  heart 
cases  with  a .  nervous  element  where  they  will  associate  as  much  as  pos- 
sible with  healthy  people,  whose  pursuits  and  tastes  do  not  lean  towards 
introspection. 


APPENDIX  I 

The  Pulse  in  Angina  Pectoris 

The  condition  of  the  arterial  system  immediately  before  and  during  an 
attack  of  angina  pectoris  has  been  the  subject  of  a  good  deal  of  speculation, 
and  a  good  many  h3rpotheses  in  regard  to  diagnosis  and  treatment  have  been 
based  upon  the  conditions  that  are  supposed  to  exist.  Unfortunately,  very 
few  observations  have  been  made  to  determine  the  actual  condition,  and 
those  that  have  been  published  do  not  bear  a  very  critical  examination.  It 
is  only  at  unexpected  times  that  one  has  the  opportunity  for  making  the 
observation,  and  the  circumstances  are  rarely  suited  for  making  these  suffi- 
ciently accurate.  I  have  been  somewhat  fortunately  circumstanced  for 
this  purpose.  For  many  years  while  I  was  in  Burnley  I  had  been  consulted 
by  large  numbers  of  people  with  affections  of  the  heart.  Three  of  the  four 
roads  that  led  past  my  house  were  steep,  and  the  patients  suffered  in  climbing 
the  hill.  Not  infrequently  in  my  consulting  room,  or  in  my  waiting  room, 
patients  would  be  seized  with  attacks  of  angina  pectoris,  and  I  have  had 
many  times  to  administer  amyl  nitrite  for  their  relief.  As  I  always  had 
my  sphygmograph  ready,  I  frequently  obtained  very  good  tracings.  I  may 
say  that  in  not  a  single  case  did  I  ever  find  any  evidence  of  vascular  spasm, 
recognizable  by  the  finger,  nor  had  I  any  difficulty  in  getting  tracings  on 
account  of  the  smallness  of  the  pulse.  While  one  cannot  always  infer 
from  the  size  of  the  tracing  that  the  radial  artery  was  large,  yet  it  does  offer 
confirmatory  evidence.  A  small  deformed  tracing  may  easily  be  got  from 
a  large  radial  pulse,  by  hasty  and  inaccurate  adjustment  of  the  instrument, 
but  it  is  rare  to  get  a  large  tracing  from  a  small  contracted  artery,  and 
I  give  the  following  tracings  merely  as  corroborating  the  sensations  imparted 
to  my  finger. 

In  tracings  taken  before  and  after  the  administration  of  amyl  nitrite, 
the  size  of  the  artery  and  the  character  of  the  tracing  showed  very  little 
difference.  During  the  administration  there  was  always  the  characteristic 
changes — increased  rapidity  and  lowering  of  the  dicrotic  notch,  as  in  Fig. 
169.  It  may  be  said  that  the  attacks  in  the  cases  cited  were  after  bodily 
exertion  had  exhausted  the  heart,  and  that  the  attacks  that  come  on  when 


THE  PULSE  IN  ANGINA  PECTORIS 


303 


the  patient  is  at  rest  may  be  due  to  arterial  spasm.  I  have  also  had  occasion 
to  see  a  good  number  of  cases  who  suffered  from  attacks  while  in  bed,  and 
here  likewise  I  detected  no  arterial  spasm.  In  a  few  cases  I  have  found  the 
arterial  pulse  small  during  an  attack,  and  in  one  case  imperceptible  ;  but 
these  were  cases  of  extreme  exhaustion  of  the  heart,  with  very  feeble  heart 
sounds,  and  the  administration  of  amyl  nitrite  had  no  effect.  Two  of 
these  patients  died  a  few  hours  after  my  examination. 


Fig.  168.     Large  alternating  pulse  during  an  attack  of  angina  pectoris.    B.P.  190.    (Case  1. 
Figs.  169  and  170  are  from  the  same  patient.) 

I  have  a  large  amount  of  material  to  select  from,  but  I  limit  myself  to 
a  few  cases  of  the  most  severe  type. 

Case  1. — Male,  aged  52  (whose  case  is  described  more  fully  later — Case  23, 
Appendix  V).  Had  suffered  two  years  from  breathlessness.  As  he  had 
a  well-marked  pulsus  alternans  I  have  made  a  large  number  of  observa- 
tions on  him.  His  condition  fluctuated  very  much.  During  a  period  when 
he  was  worse  than  usual  he  called  to  see  me,  walking  up  a  steep  hill  on 


Fig.  169.     Under  amyl  nitrite.     (Case  1.) 

the  way.  He  began  to  feel  a  tightness  across  his  chest  which  developed 
into  a  severe  pain.  I  examined  him  and  took  a  tracing  of  his  pulse 
(Fig.  168).  I  took  his  blood-pressure  and  found  it  190  mm,  Hg.  His 
pulse  did  not  alter  in  character  during  his  suffering,  and  the  height  of  the 
waves  showed  that  there  was  no  contraction  of  the  artery,  nor  did  it  differ 
in  character  from  the  pulse  tracing  taken  when  he  was  free  from  pain. 
I  gave  him  amyl  nitrite  to  inhale,  the  pulse  quickened  (Fig.  169),  and  the 
amyl  nitrite  gave  him  instant  relief.  Fifteen  minutes  after  he  was  quite 
free  from  pain,   his   blood-pressure  had  risen  to    200  mm.  Hg.,  and  the 


304 


DISEASES  OF  THE  HEART 


alternating  character  of  the  rhythm  became  more  marked  (Fig.  170).  In 
the  post-mortem  account  of  the  patient  it  will  be  shown  that  there  was 
extensive  fibrosis  of  the  heart  muscle,  and  disease  of  the  coronary  artery. 

Case  2. — Female,  aged  60  ;  complained  of  pain  in  her  chest,  radiating 
into  the  left  arm,  and  persisting  in  the  left  fore-arm  with  great  severity.  It 
was  easily 'induced  by  exertion,  and  one  day  when  coming  to  see  me  she 
had  hurried.  While  I  was  examining  her  the  pain  seized  her  with  great 
violence.    I  took  tracings  of  her  radial  and  jugular  pulses.    The  heart's  rate- 


Fig.  170.  Fifteen  minutes  after  the  inhalation  of  amyl  nitrite  and  after  cessation  of  the 
anginal  symptoms  the  alternating  character  of  the  pulse  became  more  marked,  and  the  blood- 
pressure  of  the  larger  beats  had  risen  to  200  mm.  Hg.     (Case  1.) 

was  increased  but  the  radial  pulse  was  of  a  good  size  (Fig.  171).  I  gave  her 
amyl  nitrite  and  it  relieved  the  pain  at  once.  The  patient  died  three  months 
after  from  heart  failure,  and  Dr.  R.  T.  Williamson  examined  the  heart  for 
me  and  found  marked  atheroma  and  calcification  of  the  coronary  arteries 
and  extensive  fibrous  changes  in  the  muscle  of  the  left  ventricle. 

Case  3. — Male,  52.  Mechanical  engineer  ;  was  going  to  his  work  on 
March  14,  1903,  when  he  was  seized  with  a  severe  pain  across  his  chest  and 


Fig.  171.     Taken  during  an  attack  of  angina  pectoris — the  radial  pulse  is  seen  to  be  of  good 

size.     (Case  2.) 

called  on  me.  I  found  him  suffering  great  agony  ;  his  face  ashen  in  colour, 
his  pulse  full  and  regular  (Fig.  172).  I  gave  him  first  amyl  nitrite  with  no 
effect  on  the  pain,  then  a  hypodermic  injection  of  |  grain  of  morphia.  This 
gave  him  relief.  The  heart's  dullness  was  normal,  but  the  sounds  were  soft 
and  there  was  a  murmur  after  the  first  sound.  After  a  week's  rest  the 
patient  improved  and  resumed  his  work,  but  on  January  15,  1905,  he  was 
again  seized  with  a  severe  attack  of  angina  pectoris.  For  some  months  after- 
wards the  pain  came  on  with  little  provocation,  and  I  saw  him  in  one  attack 


THE  PULSE  IN  ANGINA  PECTORIS 


305 


and  the  pulse  was  not  affected.  The  pains  diminished  in  severity  as  the 
heart  dilated  and  became  weaker,  dropsy  and  oedema  of  the  lungs  super- 
vened and  he  died  on  June  1,  1905.  Dr.  Keith's  report  of  the  heart  stated 
that  the  coronary  arteries  showed  a  slight  thickening  of  the  intima,  but 
the  muscle  coat  was  hypertrophied  ;  thickening  of  the  mitral  cusps  but  no 
stenosis  ;  the  foramen  ovale  was  slightly  patent ;  the  right  ventricle  was 
hypertrophied  and  dilated,  while  the  left  was  dilated  and  atrophied  with 
a  considerable  degree  of  fatty  degeneration  and  a  shght  degree  of  fibrosis. 


Fig.  172.     During  an  attack  of  angina  pectoris.     (Case  3.) 

Case  4. — Male,  aged  52  at  his  death  ;  had  been  under  my  care  for  four 
years.  His  complaint  at  first  was  pain  induced  by  exertion,  starting  across 
his  chest  and  radiating  into  the  left  arm.  At  times  the  pain  was  so 
easily  excited  that  he  had  to  keep  in  bed  for  a  few  days.  On  February  8, 
1894,  he  complained,  in  addition,  of  a  pain  and  soreness  in  the  head,  which 
developed  into  severe  attacks  of  headache.  I  saw  him  in  an  attack  of 
angina  pectoris,  which  came  on  while  he  was  in  bed  on  March  19,  1894  ; 
his  pulse  was  full  and  regular,  and  there  was  no  sign  of  contracted  arteries 


Fig.  173.     During  an  attack  of  angina  pectoris.     (Case  4.) 

(Fig.  173).  I  gave  him  amyl  nitrite  without  effect  on  the  pain,  and  he  was 
only  eased  by  chloral.  He  died  in  an  attack  of  angina  on  March  27,  1894. 
Dr.  Williamson  reported  that  the  ventricles  were  soft  and  friable  ;  well- 
marked  atheroma  of  the  coronary  arteries  ;  in  many  places  the  arteries  and 
their  branches  were  calcified.  Microscopic  examination  of  the  left  ventricle 
showed  fatty  degeneration. 

Case  5. — Male,  aged  68  at  his  death.  Consulted  me  on  November  17, 
1899,  because  of  pain  over  his  chest  on  exertion.  He  was  a  millwright  by 
trade — a  big  powerful  fellow.  As  he  was  in  comfortable  circumstances 
I  advised  him  to  give  up  hard  manual  work.     He  followed  this  advice,  and 

MACKENZIE  -V" 


306 


DISEASES  OF  THE  HEART 


was  free  from  pain  until  July  8,  1902,  when  he  was  seized  with  violent  pains 
on  going  up  a  hill.  He  came  home  and  went  to  bed,  when  the  pain  returned, 
and  I  saw  him  during  an  attack  of  agonizing  severity  which  lasted  over  ten 
minutes.  While  amyl  nitrite  was  being  fetched,  I  took  tracings  of  his 
pulse  (Figs.  174  and  175).  The  amyl  nitrite  gave  him  a  little  ease,  and  the 
pain  gradually  subsided.  During  the  attack  the  character  of  the  pulse  did 
not  alter,  and  there  was  no  sign  of  contracted  arteries.      The  heart  was 


Fig.  174.     Large  irregular  pulse  during  an  attack  of  angina  pectoris.     (Case  5.) 

irregular,  due  mainly  to  extra-systoles,  sometimes  interpolated  as  in  Figs.  174 
and  175.     He  had  repeated  attacks  and  died  in  one  on  July  10,  1902. 

I  have  found  in  a  good  number  of  cases  that  the  rate  became  more 
frequent  during  attacks  of  angina  pectoris.  In  one  case  of  aortic  disease 
the  attack  of  angina  coincided  with  a  sudden  increase  in  the  rate,  of  which  I 
got  a  tracing,  but  unfortunately  it  is  lost.  There  is  often  a  tendency  to 
the  production  of  extra-systole  induced  at  the  same  time,  as  shown  in  the 


Fig.  175.     The  same  as  Fig.  174.     (Case  5.) 

two  last  tracings  (Figs.  174  and  175).      The  following  case  illustrates  this 
tendency  : — 

Case  6. — Male,  43  years  of  age  :  consulted  me  on  September  13,  1900. 
Had  good  health  until  a  year  ago,  when  he  began  to  be  short  of  breath  on 
exertion.  Shortly  after  this  he  suffered  from  a  pain  that  shot  into  his 
left  arm  when  he  exerted  himself.  Four  days  before  coming  to  me  the  pain 
struck  with  great  severity  into  his  chest  and  down  the  inside  of  the  left  arm, 
and  lasted  for  half  an  hour.     He  has  been  a  heavy  drinker.     On  the  19th 


THE  PULSE  IN  ANGINA  PECTORIS 


307 


he  called  again  upon  me  ;  was  seized  with  the  pain,  which  held  him  for  some 
minutes,  and  I  got  tracings  of  the  jugular  and  radial  pulses  while  the  pain 
was  present.     The  pulse  increased  in  rate  and  became  irregular  (Figs.  176  and 


.V^vA^V^A^iVtvlA/lAAM 


Fig.  176.     Shows  extra-systoles  occurring  during  an  attack  of  angina  pectoris.     (Case  6.) 

177).     These  irregularities  are  due  to  ventricular  extra-systoles  ;  in  Fig.  177 
the  extra-systole  is  interpolated  between  two  normal  beats. 

The  patient  improved  under  treatment,  and  I  did  not  see  him  again  after 


Fig.  177.    Shows  an  interpolated  extra-systole  during  an  attack  of  angina  pectoris.    (Case  6.) 

the  end  of  September.     He  dropped  dead  in  January,  1901,  while  watching 
a  football  match. 

Irregularities  of  a  more  obscure  kind  may  appear  during  an  attack  of 
angina  pectoris,  and  the  pulse  may  become  slow. 


Fig.  178.     Pulse  of  high  arterial  pressure  from  a  case  of  chronic  albuminuria.     (Case  7.) 

Case  7. — Female,  aged  68.  Had  been  under  my  care  for  five  years, 
suffering  from  cirrhotic  kidney.  Her  pulse  was  always  hard  and  regular 
(Fig.  178).     On  February  28,  1900.  she  was  seized  with  an  attack  of  angina 


Fig.  179.     Irregular  pulse  during  an  attack  of  angina  pectoris.     (Case  7.) 

pectoris.  These  attacks  kept  recurring,  though  she  lay  in  bed.  I  saw  her 
in  an  attack  on  the  25th  ;  her  face  was  blanched  and  shrunk,  and  damp 
with  perspiration.     The  pulse  became  very  irregular,  as  in  Figs.  179  and  180. 

x2 


308  DISEASES  OF  THE  HEART 

Relief  was  only  obtained  by  large  doses  of  opium,  vaso-dilators  having  no 
effect  (amyl  nitrite,  whisky  and  hot  water).     Next  day  she  was  better  and 


Fig.  180.  Tracing  of  radial  pulse  showing  the  appearance  of  the 
pulsus  alternans  after  a  long  pause  during  an  attack  of  angina  pectoris. 
(Case  7.) 

her  pulse  quite  regular  (Fig.  181).     She  died  in  the  following  week  during 
an  attack  of  angina  pectoris. 

The  nature  of  the  irregularity  in  Fig.  180  is  easy  to  understand.     An 


Fig.  181.     Pulse  of  the  same  patient  after  the  subsidence  of  an  attack  of  angina  pectoris. 
The  pulse  is  here  regular.     (Case  7.)         ' 

extra-systole  occurred  during  the  long  pause,  and  this  was  followed  by 
the  pulsus  alternans — an  indication  of  profound  exhaustion  of  contractility. 
I  am  not  able  to  account  satisfactorily  for  the  nature  of  the  irregularity  in 
Fig.  179. 


APPENDIX  II 

The  Nodat,  Rhythm 

The  starting  of  the  contraction  of  the  heart  at  a  place  other  than  the 
normal  is  a  conception  so  novel  in  the  physiology  of  the  heart's  action, 
and  has  such  a  profound  bearing  upon  the  diagnosis  and  treatment  of  heart 
failure,  that  it  is  necessary  to  give  the  evidence  for  this  conception  in  some 
detail.  Already  experimental  evidence  is  accumulating  in  favour  of  this 
idea,  as  shown  by  the  observations  of  Cushny^^'  (Figs.  58  and  59)  and 
Lewis  207.  Further,  the  most  accurate  of  all  methods  of  cUnical  observation, 
viz.  by  means  of  the  electro-cardiogram,  has  amply  confirmed  the  con- 
clusions I  have  drawn  from  the  study  of  the  heart  murmur  and  graphic 
records  of  the  circulatory  movements  (see  Appendix  VII).  Clinical  and 
pathological  evidences  are  given  in  this  Appendix,  the  former  full  and 
complete,  the  latter  confirmatory,  and  awaiting  further  work. 

The  cUnical  evidence  consists  in  the  disappearance  of  all  signs  of  the 
auricular  systole  occurring  at  the  normal  period  in  the  cardiac  cycle.  Such 
signs  of  normal  auricular  activity  are  : — 

(1)  A  wave  in  the  jugular  pulse  tracing  due  to  a  contraction  of  the  right 
auricle. 

(2)  A  wave  in  the  apex  tracing  due  to  a  contraction  of  the  left  auricle. 

(3)  A  wave  in  the  liver  pulse  due  to  a  contraction  of  the  right  auricle. 

(4)  A  presystolic  mitral  murmur  due  to  a  contraction  of  the  left  auricle. 

(5)  A  presystolic  tricuspid  murmur  due  to  a  contraction  of  the  right 
auricle. 

The  most  important  evidence  is  found  in  the  character  of  the  jugular 
pulse.  As  has  been  already  pointed  out,  there  is  normally  a  wave  preceding 
the  carotid  and  radial  pulse,  as  in  Fig.  183,  where  the  wave,  a,  from  its 
position  in  the  cardiac  cycle,  is  recognized  as  being  due  to  the  auricular 
systole.  When  the  nodal  rhythm  arises  the  character  of  the  venous  pulse 
at  once  changes,  and  we  get  a  form  of  venous  pulse  in  which  there  is  no 
evidence  of  an  auricular  contraction  in  the  normal  period  ;  in  other  words, 
the  jugular  pulse  changes  from  one  of  the  auricular  type  to  one  of  the  ven- 
tricular type  (§  115),  and  the  heart's  action  becomes  irregular.     PresystoHc 


310  DISEASES  OF  THE  HEART 

murmurs  due  to  the  auricle,  as  well  as  auricular  waves  in  liver  and  apex 
tracings,  disappear. 

In  the  clinical  history  of  the  cases  cited  I  will  only  refer  to  the  evidence 
bearing  upon  the  matter  in  hand.  These  cases  are  selected  to  show  that 
every  one  of  the  above-mentioned  signs  of  auricular  activity  disappear. 

I  have  now  collected  records  of  nearly  600  cases  of  nodal  rhythm,  and  a 
careful  analysis  of  these  leads  me  to  conclude  that  there  are  a  number  of  dis- 
tinct varieties.  Most  of  these  I  am  unable  yet  to  classify  with  sufficient  pre- 
cision, but  I  entertain  no  doubt  that  with  extended  experience  and  improved 
methods  this  classification  will  be  ultimately  attained.  One  small  class 
stands  out  from  the  others  very  clearly.  In  the  majority  of  cases  of  nodal 
rhythm  the  rate  of  the  heart-beat  is  increased,  sometimes  extremely  so. 
In  a  few  cases  it  is  found  slower  than  normal,  sometimes  markedly  so. 
These  cases  of  infrequent  rate  I  place  in  a  separate  class  and  describe  them 
under  the  term  Nodal  Bradycardia  (Appendix  IV). 

I  had  hoped  to  have  been  able  to  give  a  fairly  full  account  of  the  patho- 
logical condition  in  cases  of  the  nodal  rhythm,  but  I  find  there  is  a  vast 
amount  of  pioneer  work  still  to  be  done,  and  the  pathological  results  given 
here  are  put  forward  with  all  reserve  and  are  suggestive  rather  than  con- 
clusive. Monckeberg  ^i-  has  recently  published  a  book  on  the  pathology  of 
the  auriculo-ventricular  bundle,  but  the  clinical  records  are  so  scanty  that 
no  clear  perception  can  be  obtained  of  the  symptoms  during  life,  but,  so 
far  as  I  can  see,  his  observations  seem  to  confirm  those  of  Keith  given  here. 
For  some  years  I  have  sent  to  Professor  Keith  hearts  affected  with  many 
forms  of  disease.  He  has  examined  these  without  knowing  the  clinical 
histories.  On  comparing  his  descriptions  with  the  clinical  notes,  I  found, 
with  one  exception,  that  all  cases  that  had  the  nodal  rhythm  during  life 
presented  some  evidence  of  change  in  the  primitive  cardiac  tissue,  or  in  the 
artery  supplying  it.  There  were  also  found  such  changes  in  the  auricular 
wall  in  a  few  cases  as  to  suggest  an  interruption  of  the  means  of  com- 
munication between  the  sino-auricular  and  auriculo-ventricular  nodes 
(Fig.  2).  The  exceptional  case  I  have  subsequently  found  to  belong  to 
a  different  category  (nodal  bradycardia.  Case  22). 

I  would  particularly  draw  attention  to  Cases  11  and  12,  which  repre- 
sent typical  instances  of  paroxysmal  tachycardia,  the  one  secondary  to 
rheumatic  sclerosis,  and  the  other  associated  with  arterial  degeneration. 
The  pathological  conditions  found  in  these  cases  afford  support  for  the  view 
put  forth  that  the  a.-v.  node  or  bundle,  by  the  invasion  of  the  diseased 
processes,  is  rendered  more  irritable  than  the  sinus  remains,  and  on  account 
of  its  excessive  irritability  starts  the  rhythm  of  the  heart. 


THE  NODAL  RHYTHM 


311 


Before  entering  into  a  detailed  account  of  the  cases,  there  are  two  points 
to  which  it  may  be  useful  to  refer  for  the  help  of  those  who  may  follow  this 
line  of  inquiry.  In  many  cases  it  will  be  found  that  when  the  radial  pulse- 
beats  are  very  small  or  occasionally  absent,  the  jugular  or  liver  pulse  may 
be  large,  as  in  Figs.  66,  158,  160,  and  209.  The  reason  for  this  is  that  the 
force  opposing  the  contraction  of  the  left  ventricle  (the  aortic  pressure)  is  so 
great  that  the  ventricular  contraction  is  barely  able  to  overcome  it.  On  the 
other  hand,  the  force  opposing  the  backward  flow  through  the  incompetent 
tricuspid  orifice  is  so  sHght  (the  pressure  in  the  great  veins)  that  the  right 
ventricle  has  no  difficulty  in  overcoming  this  pressure  even  with  a  feeble 
contraction. 


2,         a               3               3                  V 
Jugular                                                                                ^ 

3              3              3                         1 

^.          1              1 

^^^"^""^  r           "^^-^-^                                     /     ^ — ~-,^        /                  '   'fc-,^/'^- — ,          -"^^^                                              J                "'^s.-.^^  Lf—- *^^  _                    X       "'*'*^.^            y'""            ■»»           1 

^rorid                                                                                                   '                                                               1 

Fig.  182.  At  x  and  x '  a  series  of  waves  is  shown  which  were  produced  by  partial  com- 
pression of  the  vein  by  the  receiver.  The  stream  of  blood  passing  through  the  narrowed 
lumen  caused  a  perceptible  thrill  in  tlie  surrounding  structures,  and  produced  vibrations  of  the 
tambour  wMch  are  registered  as  waves  in  the  tracing.  With  care  the  tracing  can  be  obtained 
free  from  these  artificial  waves,  as  in  Fig.  53,  which  was  taken  from  the  same  patient. 

I  have  in  a  few  cases  of  nodal  rhythm  found  in  the  tracings  during 
ventricular  diastole  a  series  of  small  waves.  In  the  first  few  cases  I  sought 
carefully  to  see  that  there  was  not  some  error  in  the  method,  and  failing  to 
find  any  fault  I  inferred  that  these  waves  were  due  to  fibrillation  of  the 
auricle,  and  I  have  so  described  them  in  one  or  two  published  articles. 
From  one  patient  with  a  large,  full,  jugular  vein  I  obtained  sometimes  very 
large  waves  during  a  long  pause,  as  at  x  in  Fig.  182.  When  I  carefully 
inspected  this  vein  I  found  that  when  I  partially  compressed  the  vein  with 
my  finger  perceptible  thrills  in  the  surrounding  structures  were  produced, 
because  the  blood  was  flowing  through  the  constricted  vein.  From  this 
observation,  I  now  recognize  that  what  I  had  taken  for  waves  due  to  fibril- 
lation of  the  auricle  may  in  some  instances  have  been  due  to  a  fault  in  the 
method  of  registration,  wherein  by  compressing  the  vein  with  the  receiver 
I  had  artificially  produced  thrills  which  appeared  as  waves  in  the  tracing. 


312 


DISEASES  OF  THE  HEART 


Other  waves  due  to  the  same  cause  are  apt  to  appear,  and  if  the  cause  be 
not  recognized  it  might  be  assumed  that  the  waves  were  due  to  the  auricle, 
as  at   x' in  Fig.  182. 

Case  7. — Sudden  inception  of  the  nodal  rhythm  shown  by  the  disappear- 
ance of  the  auricular  wave  from  the  jugular  pulse,  and  of  the  presystolic  mitral 
murmur,  with  the  appearance  of  permanent  irregularity  in  the  heart's  action,  and 


Fig.  183.  Simultaneous  tracings  of  the  jugular  and  radial  pulses  in  the  first  part,  of  the 
carotid  and  radial  in  the  latter  part.  The  jugular  tracing  shows  the  form  characteristic  of  the 
auricular  venous  pulse  where  the  wave,  a,  due  to  the  auricle  precedes  the  carotid  wave,  c  (down- 
stroke  3).  The  shading  underneath  represents  the  time  of  the  presystolic  murmur.  (Case  7, 
November  5,  1895). 

ventricular  form  of  the  venous  pulse.    Post-mortem  evidence  of  disease  affecting 
the  remains  of  the  primitive  cardiac  tissue. 

Female,  born  1864.  I  first  saw  this  patient  in  1895,  she  being  then 
thirty-one  years  of  age.  There  was  a  history  of  acute  rheumatism  in  her 
youth,  and  she  had  marked  mitral  stenosis.    She  became  pregnant  in  1896, 


Fig.  184.     The  jugular  pulse  is  now  of  the  ventricular  form — no  auricular  wave  precedes 
the  downstroke  3,  and  the  rhythm  is  irregular.     (Case  7,  March  19,  1904.) 

and  I  watched  her  during  the  pregnancy  and  puerperium.  She  had  a  long 
illness  from  gastric  ulcer  in  1899.  During  these  years  I  made  frequent 
observations  on  her  heart.  It  was  invariably  regular,  and  the  jugular  pulse 
always  showed  a  well-marked  wave  due  to  the  systole  of  the  right  auricle. 
There  was  at  first  a  presystolic  mitral  murmur  of  the  crescendo  type,  and 
latterly  a  long  murmur  following  the  second  sound  and  running  up  to  the 
crescendo  presystolic  murmur.  The  position  of  the  presystoUc  murmur  in 
the  cardiac  cycle  is  diagrammatically  represented  in  the  shading  under  the 
radial  tracing  in  Fig.    183.     This  perfect  regularity  of  the  heart's  action 


THE  NODAL  RHYTHM 


313 


continued  until  she  suffered  from  an  attack  of  heart  failure  in  1900. 
Coincident  with  this  failure  the  heart's  action  became  irregular,  and  the 
jugular  pulse  showed  no  sign  of  a  wave  due  to  the  auricular  systole  at  the 
normal  period  of  the  cardiac  cycle  (Fig.   184).     The  crescendo  presystolic 


Fig.  185.     The  jugular  pulse  is  of  the  ventricular  form,  and  a'  is  probably  due  to  the  auricular 
systole  occurring  at  the  same  time  as  the  ventricular.    (Case  7,  December,  1906.) 

murmur  had  disappeared,  while  the  diastoUc  portion  persisted,  as  shown  by 
the  shading  under  the  apex  tracing  in  Fig.  186. 

From  this  date  until  she  died  in  February,  1907,  these  altered  conditions 
persisted.  Fig.   185  being  a  simultaneous  tracing  of  the  jugular  pulse  and 


Fig.  186.     The  jugular  pulse  shows  the  same  features  as  in  Fig.  185.     (Case  7, 

February,  1907.) 

radial  taken  in  December,  1906,  and  Fig.  186  of  the  jugular  and  apex  beat 
taken  February,  1907,  shortly  before  she  died. 

Concerning  the  jugular  pulse,  it  will  be  seen  that  in  Figs.  184,  185,  and 
186,  there  is  not  the  slightest  sign  of  the  auricular  wave,  a,  at  its  normal 
period  in  the  cardiac  cycle,  which  is  so  marked  a  feature  in  Fig.  183.     The 


314  DISEASES  OF  THE  HEART 

rhythm  of  the  heart  was  sometimes  fairly  regular,  but  invariably  after  a  few 
beats  the  diastolic  period  showed  distinct  variations  in  length  ;  among 
a  large  number  of  tracings  which  have  been  taken  from  this  patient  since 
1900,  I  have  never  found  one  that  was  regular. 

The  following  is  an  abbreviated  report  on  the  post-mortem  examination 
of  the  heart  : 

Valves  :  Great  stenosis  of  the  mitral  valves  ;  tricuspid  valves  shallow 
and  incompetent ;  pulmonary  and  aortic  valves  normal.  Coronary  arteries 
healthy  ;  coronary  veins  dilated  to  twice  their  normal  diameter.  Superior 
and  inferior  vena  cavae  much  dilated.  The  sino-auricular  node  is  normal, 
but  the  auricular  wall  below  it  is  atrophied  and  fibrous.  The  taenia 
terminalis  is  h3rpertrophied.  The  auriculo-ventricular  bundle  has  partly 
assumed  the  characters  of  the  ordinary  muscular  fibres,  and  has  been 
stretched,  and  the  a. -v.  node  is  flattened  by  the  great  inter-auricular 
pressure.  The  central  fibrous  body  is  marked  (fibrous  and  contracted), 
and  the  artery  perforating  it  is  atheromatous.  The  apical  half  or  two- 
thirds  of  the  left  ventricle  shows  extensive  fibrosis.  The  fibrotic  process 
approaches  and  incorporates  the  musculature  along  a  sharply  defined 
line.  In  the  fibrotic  tissue  are  nodules  characteristic  of  rheumatic  con- 
ditions. Since  the  fibrotic  process  is  most  marked  at  the  base  of  the 
musculi  papillares,  it  is  possible  that  it  may  have  spread  from  the  mitral 
valves. 

Case  8. — Sudden  inception  of  the  nodal  rhythm,  shown  by  the  disappear- 
ance of  the  auricular  wave  from  the  liver  pulse,  and  of  the  presystolic  mitral 
murmur,  with  the  appearance  of  permanent  irregularity  in  the  heart's  action 
and  ventricular  form  of  the  liver  pulse.  Post-mortem  evidence  of  the  invasion 
of  the  primitive  cardiac  tissue  by  the  diseased  process. 

Female,  born  1851,  came  under  my  care  in  1880.  She  had  had  rheumatic 
fever  in  childhood,  and  had  suffered  from  mitral  stenosis,  there  being  a  well- 
marked  presystolic  murmur.  In  1880  and  1882  I  attended  her  for  attacks 
of  rheumatic  fever.  In  1892  there  was  considerable  enlargement  of  the 
liver,  which  pulsated  (Fig.  187). 

The  character  of  the  pulsation  being  of  the  auricular  type,  I  concluded 
that  there  was  also  tricuspid  stenosis,  a  diagnosis  which  was  afterwards 
verified  at  the  post-mortem  examination.  Occasionally  I  detected  an 
extra-systole.  Fig.  189,  which  Fig.  190  shows  to  be  due  to  premature  con- 
traction of  the  ventricle.  Tliis  characteristic  pulsation  of  the  liver  continued 
until  1898  (Fig.  188,  for  instance,  being  taken  in  1897),  when  she  had  an 
attack  of  heart  failure,  during  which  time  her  pulse  was  rapid  and  irregular 
(Fig.  191). 


THE  NODAL  RHYTHM 


315 


When  the  heart  had  quieted  down  the  tracing  showed  a  complete  absence 
of  the  wave  due  to  the  auricular  systole  (Fig.  192),  and  the'  presystolic 
murmur  had  disappeared. 


Fig.  187.     The  liver  pulse  shows  a  well-marked  wave  (a)  due  to  the 
auricle.     (Case  8.     1892.) 


Fig.  188.    There  is  still  a  well-marked  wave  in  the  auricle.    (Case  8.     1897. ) 


Fig.  189.     Shows  an  extra-systole.     (Case  8.) 


Fig.  190.  Simultaneous  tracings  of  the  apex  beat  and 
of  the  liver  pulse,  showing  the  rhytlimical  contraction  of 
the  auricle,  a',  while  there  is  a  premature  beat  in  the  apex 
(ventricular  extra-systole).     (Case  8.) 

This  patient  lived  until  1899,  and  in  the  numerous  tracings  taken  up 
to  her  death  the  rhythm  was  never  again  found  regular,  nor  was  there 
present  either  the  presystolic  murmur  or  the  wave  in  the  liver  pulse  due  to 


316  DISEASES  OF  THE  HEART 

the  auricle.  Here,  again,  the  irregularity  in  the  action  of  the  heart  was 
coincident  with  the  disappearance  of  all  signs  of  auricular  systole,  namely, 
the  disappearance  of  the  auricular  wave  from  the  liver  pulse,  showing  the 
cessation  of  the  action  of  the  right  auricle,  and  the  disappearance  of  the  pre- 
systoHc  murmur,  showing  the  cessation  of  the  action  of  the  left  auricle. 

The  report  of  the  post-mortem  examination  of  the  heart  is  as  foUows  : — 
Extreme  stenosis  of  mitral  and  tricuspid  orifices  ;  great  dilatation  of  auricles, 


Fig.  191.  Sudden  inception  of  the  nodal  rhythm,  showing 
increased  frequency  of  the  heart's  action,  irregularity  and  dis- 
appearance of  the  auricular  wave  from  the  liver  pulse.  (Case  8. 
1898.) 

with  atrophy  of  the  musculature.  There  is  a  large  nodular  mass  of  endo- 
cardial thickening  showing  calcareous  masses  in  its  centre,  and  active 
inflammatory  proliferation  at  its  periphery,  on  the  endocardium,  under  the 
aortic  orifice,  and  situated  in  the  pars  membranacei  septi  right  over  the  a.-v 
bundle.  At  one  point  the  inflammatory  extension  has  invaded  and  involved 
a  great  part  of  the  bundle.     The  stretching  of  the  bundle  is  extreme,  and 


Fig.  192.  When  the  heart  became  slower  the  nodal  rhythm  persisted.  When  compared 
with  Figs.  187  and  188,  it  will  be  seen  tliat  there  is  no  auricular  wave  in  the  liver  pulse,  and 
the  heart's  action  is  irregular.     (Case  8.     1898.) 

there  is  cell  proHferation  which  Professor  Keith  regards  as  due  to  changes 
in  the  walls  of  the  small  vessels. 

There  is  extreme  atrophy  of  the  upper  part  of  the  inter-ventricular 
septum.  It  measures  only  4  mm.  instead  of  14-18.  The  sub-endocardial 
tissue  is  thickened,  and  in  parts  the  Pur  kin  je  system  is  fibrosed  and  atrophied. 

Case  9. — Disappearance  of  large  auricular  waves  from  the  venous  pulse  with 
the  onset  of  continued  irregular  action  of  the  heart.     Fibrosis  of  the  a.-v.  bundle. 

Female,  born  1850  ;  enjoyed  good  health  till  1900,  when  she  began  to 
be  short  of  breath.     I  saw  her  first  in  November,    1902.     She  was  then 


THE  NODAL  RHYTHM  317 

very  weak,  and  had  to  lie  in  bed  propped  up  ;  the  legs  and  abdomen  were 
swollen  and  the  urine  scanty  ;  the  pulse  was  small,  weak,  and  regular,  and 
there  was  a  large  pulsation  in  the  veins  of  the  neck  (Fig.  193).  The  heart's 
dullness  extended  two  inches  to  the  right  of  the  mid-sternal  line,  and  one 
inch  to  the  left  of  the  nipple  line.  The  sounds  were  clear  and  free  from 
murmur. 


Fig.  193.     Shows  a  well-marked  auricular  wave  in  the  jugular  tracing  during  an  attack 
of  extreme  heart  failure.     (Case  9.     1902.) 

Under  treatment  she  improved  very  much,  the  pulse  becoming  slower 
(Fig.  194),  but  she  had  several  relapses,  until  the  final  breakdown  in  November, 
1904,  Figs.  193  and  194  are  tracings  of  the  radial  pulse  and  jugular  pulse 
taken  in  1902.  The  jugular  pulse  is  of  the  auricular  form,  and  the  rhythm 
there  is  perfectly  regular.  I  took  a  large  number  of  tracings  at  different 
times  up  till  November,    1904,  and  the  rhythm  was  invariably  regular, 


Fig.  194.     .Shows  a  well-marked  auricular  wave  (a)  in  the  jugular  tracing.     (Case  9.     1902). 

and  the  jugular  pulse  of  the  auricular  type.  On  one  occasion  after  digitalis 
she  developed  a  pulsus  alternans  (Figs.  164  and  165).  The  breakdown 
at  the  last-mentioned  date  was  the  most  severe  she  ever  had,  the  legs  and 
abdomen  being  enormously  swollen  and  the  pleural  cavities  containing 
a  large  quantity  of  fluid.  The  pulse  was  now  continuously  irregular,  and 
the  venous  pulse  had  completely  changed  its  character,  being  of  the  ventri- 
cular form  (Fig.  195).  She  died  in  December,  1904,  two  months  after  I  had 
detected  the  presence  of  the  nodal  rhythm. 


318 


DISEASES  OF  THE  HEART 


The  report  on  the  post-mortem  examination  of  the  heart  is  as  follows  : — 

Greater  part  of  auricle  has  been  left  behind  in  subject. 

The  right  ventricle  is  of  quite  average  length  and  atrophied  ;  left  ven- 
tricle is  of  quite  average  length  and  dilated  and  atrophied. 

Arteries. — Show  patches  of  thickening  and  dilatation,  but  nowhere  is 
lumen  so  reduced  as  to  greatly  impede  circulation.  Aorta  shows  patches 
of  atheroma. 


Fig.  195.  Simultaneous  tracings  of  the  radial  and  jugular  pulses  taken  on  November  9, 
1904.  The  jugular  pulse  is  now  of  the  ventricular  type,  and  the  rise  in  the  jugular  during  the 
ventricular  systole  (space  E)  is  in  marked  contrast  to  the  fall  during  tliis  period  in  Fig.  194. 
There  is  no  wave  due  to  the  auricle,  and  the  rhythm  is  continuously  irregular  (nodal  rhythm). 
(Case  9.     1904.) 


Orifices  and  Valves. — Valves  healthy;  mitral  orifice  29  mm.  diam., 
tricuspid  30  mm.,  both  dilated. 

Musculature. — There  is  atrophy  and  perivascular  fibrosis  ;  this  is 
extensive  in  basal  part  of  left  ventricle,  especially  at  upper  border  of  inter- 
ventricular septum,  but  elsewhere  fibrotic  changes  not  marked. 


Fig.  196.     Radial  tracing  showing  small  beats  due  to  the  premature  contraction  of  the 
ventricle  (extra-systoles).     (Case  10.     1892.) 

A.-v.  system. — The  network  at  beginning  of  bundle  is  normal  in  size  and 
form,  although  certain  cells  which  seem  inflammatory  in  nature  are  present. 
The  bundle,  on  the  other  hand,  is  stretched  and  small,  the  fibres  show  no 
reticular  structure,  and  in  parts  show  fibrosis.  The  Purkinje  system  is 
overlaid  by  a  very  thick  fibrous  endocardium.  There  is  a  marked  degree 
of  stretching  of  the  apical  half  of  the  left  ventricle,  and  the  trabeculae  are 
thin  and  atrophied  ;  on  section,  some  of  the  Purkinje  fibres  are  seen  to  be 
undergoing  fibrous  changes. 


THE  NODAL  RHYTHM 


319 


Case  10. — Frequent  extra-systoles  from  1892  till  1906.  Signs  of  contrac- 
tion of  the  left  auricle  in  the  apex  tracings  and  of  the  right  auricle  in  the 
jugular.  Sudden  disappearance  of  these  signs  of  auricular  activity  on  the 
inception  of  the  nodal  rhythm  in  1906. 

Female,  born  1840  ;  came  under  my  care  on  May  1,  1892,  complaining 
of  weakness,  shortness  of  breath,  and  depression.     The  radial  pulse  was 


Fig.  197.  Shows  premature  contractions  of  tlie  ventricle,  o  (extra-systoles),  in  the  apex 
tracing,  wliile  in  the  jugular  tracing  are  sIiowti  waves,  a',  due  to  the  auricular  systole  occurring 
at  the  same  time  as  the  premature  ventricular  contractions.     (Case  10.     1892.) 

large  and  sHghtly  collapsing  ;  there  was  capillary  pulsation  on  rubbing 
the  forehead,  and  pulsation  in  the  jugular  vein.  The  heart  rhythm  was 
frequently  interrupted  by  extra-systoles,  Fig.  196,  and  during  the  occurrence 
of  an  extra-systole  a  big  wave  appeared  in  the  vein.  Simultaneous  tracings 
of  the  jugular  pulse  and  of  the  apex  showed  these  extra-systoles  to  be  due 
to  the  premature  contraction  of  the  ventricle.     (Fig.  197). 


B^BP^^^^^^^^^^^^^^^^^^^^^^^^^^^^B^^^^^^^^^^^^^^^^^^^^^^B 

Fig.  198.    Shows  well-marked  auricular  waves  (a)  in  the  jugular  and  apex  tracings.    (Case  10). 

The  heart  was  only  slightly  enlarged,  and  there  was  a  faint  systolic  and 
a  well-marked  diastolic  murmur  in  the  aortic  area. 

This  patient's  condition  varied  very  much  during  the  later  years  of 
her  life.  She  suffered  greatly  at  times  from  severe  attacks  of  angina 
pectoris,  but  no  change  could  be  detected  in  the  rhythm  of  the  heart. 
At  other  periods  the  extra-systoles,  like  those  in  Figs.  196  and  197,  were 


320 


DISEASES  OF  THE  HEART 


very  frequent.  The  jugular  pulse  was  invariably  of  the  auricular  type 
as  shown  in  Fig.  198.  In  the  apex  tracings  Figs.  197  and  198  there  are 
shown  well-marked  auricular  waves  {a),  due  to  contraction  of  the  left 
auricle. 

In  July  of  1906  she  was  seized  with  breathlessness  and  great  prostration. 
I  found  the  heart  extremely  rapid  and  irregular  in  its  action  (Figs.  199, 
205,  Plate  II,  and  206,  Plate  III).  She  regained  a  certain  amoimt  of  strength 
when  the  heart  slowed  down,  which  it  did  after  a  couple  of  months,  and 
Fig.  200  is  a  tracing  of  the  apex  and  jugular  taken  in  November,  1906,  and 
Fig.  208,  Plate  III,  is  a  tracing  of  the  radial  and  jugular  taken  at  the  same 
time.  The  heart  never  dilated  very  much,  and  there  was  never  any  dropsy, 
but  she  died  from  exhaustion  in  February,  1907.  Figs.  198  and  200  are 
simultaneous  tracings  of  apex  beat  and  jugular  pulse,  and  the  contrast  in 


Fig.  199.     Rapid  irregular  pulse  due  to  the  sudden  inception  of  the  nodal  rhythm. 

July,  1906.) 


(Case  10, 


the  two  tracings  is  very  marked.  In  Fig.  198  the  rhythm  is  regular  and 
there  is  a  wave,  due  to  the  left  auricle,  in  the  apex  tracing,  and  a  wave, 
due  to  the  right  auricle,  in  the  jugular  tracing.  In  Fig.  200  there  is  no 
sign  of  the  movement  of  auricle  either  in  apex  or  jugular  tracing  and  the 
rhythm  is  irregular.  Figs.  199,  205  Plate  II,  and  206  Plate  III  are 
characteristic  examples  of  the  heart  rhythm  and  rate  on  the  sudden  inception 
of  the  nodal  rhythm  in  many  cases. 

Case  11. — Transient  attacks  of  nodal  rhythm  {paroxysmal  tachycardia), 
slight  at  first,  but  becoming  permanent  and  causing  death.  Post-mortem 
examination  showed  involvement  of  the  a.-v.  bundle  in  the  disease  process. 

Male,  born  1860.  This  patient  first  consulted  me  in  January,  1900.  He 
had  an  attack  of  rheumatic  fever  at  fourteen  years  of  age.  In  1896,  after 
walking  for  twenty  minutes  at  a  rapid  pace,  he  felt  extremely  weak  and 
exhausted.  After  this  he  was  always  short  of  breath  on  exertion.  A  year 
later,  immediately  after  throwing  a  cricket  baU,  he  felt  the  heart  flutter  for 
a  few  seconds.  Ten  minutes  after  this  the  heart  '  fluttered  and  beat  quickly 
for  six  or  seven  hours  '.     He  has  had  an  attack  of  this  kind  every  two  or 


THE  NODAL  RHYTHM 


321 


three  weeks  since.  These  attacks  last  from  a  few  minutes  to  thirty  hom-s. 
At  first  he  could  sometimes  stop  the  attack  by  bending  down  and  taking 
a  deep  breath,  but  this  does  not  act  now.  Sometimes  he  passes  a  large 
quantity  of  clear  urine  in  the  course  of  an  attack.  During  an  attack,  if  in 
bed,  he  feels  exhausted  and  limp,  if  walking  he  is  easily  tired,  and  if  he  has 
to  work  for  some  hours  he  feels  swollen  round  the  waist  and  very  sore  over 
the  upper  part  of  his  abdomen,  and  feels  pain  sometimes  very  severe  across 
the  back  under  the  shoulder-blades.  During  the  night  the  sleep  is  disturbed. 
The  pulse  during  these  attacks  has  varied  under  my  observation  from 
one  hundred  and  seventy  to  two  hundred  and  twenty  beats  per  minute. 
When  the  heart  is  acting  quietly  a  short  presystoUc  murmur  at  the  apex 
and  also  a  soft  diastolic  murmur  over  the  middle  of  the  sternum  can 
occasionally  be  detected.     It  often  happens  that  these  murmurs  cannot  be 


Fig.  200.     Here  there  is  no  sign  of  an  auricular  wave  in  either  jugular  or  apex  tracing. 
Compare  the  jugular  and  apex  tracings  with  Figs.  197  and  198.    (Case  10,  November,  1906.) 

perceived.  On  producing  shght  redness  by  rubbing  the  forehead,  the  capillary 
pulsation  can  be  readily  seen.  Occasionally  the  pulse-rate  falls  to  forty- 
eight  beats  per  minute.  Towards  the  end  of  an  attack,  irregularity  of  the 
pulse  has  been  detected,  due  to  exhausted  contractility  (pulsus  alternans) 
(Fig.  130).  The  patient  (who  was  a  very  intelligent  man)  stated  that  some- 
times when  the  attack  of  rapid  heart-action  ceased  the  heart  gave  three 
or  four  violent  beats  at  intervals  longer  than  the  usual  pulse-rate.  The 
patient  died  on  November  21,  1900.  During  the  last  four  months  the 
pulse-rate  continued  rapid  for  days  together,  during  which  time  he  would 
lie  prostrate  and  exhausted.  Sleep  could  only  be  got  by  large  doses  of 
morphia.  During  the  last  two  weeks  of  his  Ufe  the  heart  acted  slowly  only 
at  rare  and  brief  intervals.  Signs  of  heart  failure  quickly  supervened — the 
face  swollen  and  livid,  and  general  oedema. 

It  is  only  necessary  here  to  call  attention  to  the  pulsation  in  the  liver  and 
in  the  veins.    I  have  made  many  observations  on  this  patient  during  numerous 

MACKENZIE  Y 


322 


DISEASES  OP  THE  HEART 


attacks  of  paroxysmal  tachycardia.  When  he  was  free  from  the  attack 
only  the  faintest  movement  could  be  detected  in  the  jugular  bulb,  and,  as 
Fig.  201  shows,  there  is  only  a  slight  wave  preceding  the  carotid  pulse.  I  was 
fortunate  enough  one  day  to  see  him  \\dthin  five  minutes  after  an  attack  began. 
The  pulse  at  first  was  not  excessively  rapid,  and  the  carotid  pulsation  was 
fairly  evident,  and  I  took  a  tracing  (Fig.  202)  of  the  carotid  immediately  above 
the  clavicle,  from  the  situation  from  which  the  jugular  pulse  in  Figs.  201 
and  204  was  afterwards  obtained.     In  Fig.  202  it  will  be  noted  that  no  sign 


Fig.  201.     Tracings  of  a  slight  movement  in  the  jugular  vein  taken  at  the  same  time  as  the 
radial  jDulse.     The  wave  a  is  due  to  the  systole  of  the  right  auricle.     (Case  11.) 

of  the  jugular  pulse  is  present.  This  would  imply  that  at  first  the  increased 
action  of  the  heart  diminishes  the  venous  pressure,  as  usually  happens  when 
the  heart  is  quickened  from  other  causes.  The  radial  tracing  is  not  so 
good  as  I  could  have  wished  ;  still  it  shows  its  time  relation  to  the  carotid 
pulse.  When  I  saw  him  again  eighteen  hours  later  the  condition  of  affairs 
had  greatly  altered.     He  had  slept  little  aU  night  ;    he  felt  Avretched,  and 


Fig.  202.  Simultaneous  tracings  of  the  carotid  (ujiper  tracing)  and  radial 
pulses  at  the  beginning  of  an  attack  of  paroxysmal  tachycardia.  The  carotid 
pulse  was  obtained  immediately  above  the  clavicle,  from  the  same  place  that 
the  jugular  pulses  in  Figs.  201,  203,  and  204  were  obtained.     (Case  11.) 

complained  of  great  pain  in  the  upper  part  of  the  abdomen  and  behind 
about  the  level  of  the  eighth  dorsal  vertebra.  His  face  had  a  wan  and  weary 
look,  and  was  of  a  greyish  colour.  Above  the  inner  end  of  the  clavicles  on 
both  sides  there  was  now  visible  a  large  and  distinct  pulsation.  If  one  care- 
fully palpated  this  part  a  distinct  pulsating  tumour  could  be  felt.  It  did  not 
extend  up  the  neck,  and  was  quite  distinct  from  the  carotid  artery.  It  was 
evidently  the  jugular  bulb  distended  by  regurgitating  waves  of  blood,  and  the 
valves  in  the  jugular  and  subclavian  veins  were  evidently  competent.  On 
auscultating  either  of  these  pulsating  tumours  or  under  the  middle  of  the 


THE  NODAL  RHYTHM 


323 


clavicle,  one  very  loud  sound  was  heard,  synchronous  with  each  pulse  beat. 
These  sounds  were  evidently  originated  by  the  sudden  and  forcible  stretching 
of  the  jugular  and  subclavian  valves.  When  I  applied  the  receiver  connected 
with  the  tambour  over  this  movement,  the  lever  was  jerked  up  with  great 
violence,  and  the  tracing  got  had  a  totally  different  character  from  that 
taken  at  the  beginning  of  the  attack.  After  taking  a  few  beats  from  the 
pulsating  jugular  bulb,  I  applied  the  receiver  over  the  carotid  in  the  middle 
of  the  neck,  and  got  the  tracing  of  the  carotid  pulse  (Fig.  203).     The  wave 


Fig.  203.  Simultaneous  tracings  of  the  pulsation  in  the  jugular  bulb  and  in  the  radial, 
and  of  the  carotid  and  radial  pulses,  during  an  attack  of  paroxysmal  tachycardia,  taken 
eighteen  hours  from  the  beginning  of  t!ie  attack.     (Case  11.) 

obtained  from  the  jugular  bulb  occurs  at  the  same  time  as  the  radial  pulse, 
and  must  therefore  be  due  to  the  ventricular  systole.  I  have  taken  a  large 
number  of  tracings  during  many  attacks,  and  they  have  all  presented  a  similar 
character.  The  tracing  Fig.  204  was  taken  after  an  attack  had  lasted 
twenty-four  hours.     It  will  be  noted  that  the  wave  here  occurs  at  the  same 


Fig.  204.     Simultaneous  tracings  of  the  radial  and  jugular  pulses  twenty-four  hours 
from  the  beginning  of  an  attack  of  paroxysmal  tachycardia.     (Case  11.) 

period  as  the  venous  tracing  in  Fig.  203.  That  this  wave  is  not  due  to  the 
carotid  can  be  seen  by  comparing  its  character  with  that  of  the  carotid  pulse 
in  Figs.  202  and  203.  One  could  convince  oneself  that  it  was  not  the  carotid 
by  examination,  the  movement  being  so  distinctly  limited  to  the  root  of 
the  neck,  while  the  carotid  above  the  pulsation  could  only  be  found  with 
difficulty.  Six  months  before  he  died  I  was  able  to  detect  slight  enlargement 
and  pulsation  of  the  liver  after  an  attack  of  tachycardia  had  lasted  fifteen 
to  twenty  hours.  During  the  last  few  weeks  of  his  life  he  was  seldom  free 
from  the  rapid  action  of  the  heart,  and  the  liver  extended  three  inches  below 

Y  2 


324  DISEASES  OF  THE  HEART 

the  ribs  and  pulsated  very  largely  (Fig.  207).  As  the  heart  became  exhausted 
the  pulse  did  not  acquire  so  great  a  rapidity  as  it  did  in  the  earlier  stages  of 
the  disease,  so  that  we  can  recognize  with  certainty  the  occurrence  of  the 
liver  pulse  during  the  ventricular  systole. 

Report  of  post-mortem  examination  of  the  heart  : — 

Coronary  artery  healthy  ;  coronary  sinus  and  veins  dilated,  but  not 
markedly  so. 

Left  auricle  greatly  dilated  and  inter-auricular  septum  greatly  stretched. 

IVIitral  orifice  =  a  linear  chink  18  x  3  mm.  Anterior  cusp  of  mitral  valve 
and  chordae  tendineae  are  the  site  of  a  warty  hard  vegetation,  the  size  of 
a  hazel-nut. 

Tricuspid  valves  healthy,  but  orifice  dilated. 

Myocardium = partial  fibrosis  in  areas.  Everywhere  the  small  vessels 
and  capillaries  are  dilated  and  the  nuclei  in  their  walls  dividing,  and  in  the 


Fig.  207.     Simultaneous  tracings  of  the  radial  and  liver  pulses  during  an 
attack  of  paroxysmal  tachycardia  towards  the  end  of  life.     (Case  11.) 

neighbourhood  of  capillaries  are  plasma  cells.  This  is  markedly  the  case 
with  the  upper  part  of  the  a. -v.  bundle  and  lower  part  of  node. 

The  sino-auricular  node  is  very  well  marked,  but  appears  in  parts  to  be 
more  fibrous  than  usual,  and  the  vessels  show  the  proliferation  of  cells  seen 
elsewhere  in  the  heart. 

The  pathological  process  which  has  affected  the  mitral  valves  spread 
up  to  the  central  fibrous  body,  and  where  the  bundle  perforates  this  there 
are  signs  of  cellular  changes  in  the  margin  of  the  bundle.  In  some  sections 
of  the  a.-v.  bundle  lower  down,  nearer  the  ventricles,  there  are  seen  in  it 
smaU  areas  from  which  the  muscular  tissue  seems  to  have  disappeared. 
There  are  thus  distinct  evidences  of  cellular  changes  in  the  bundle. 

Case  12. — History  of  many  years  of  extra-systoles,  sometimes  becoming 
very  frequent.  Transient  attacks  of  the  nodal  rhythm,  slight  at  first,  becoming 
more  prolonged  till  it  became  permanent.  Died  five  months  after  permanent 
establishment  of  the  nodal  rhythm.  Post-mortem  :  obliteration  of  lumen  of 
artery  supplying  the  a.-v.  bundle,  and  probable  disease  of  the  a.-v.  bundle. 

Female,  born  1846.  I  have  known  and  attended  her  for  slight  ailments 
at  intervals  since  1880.     In  1892  I  obtained  tracings  of  her  pulse,  which 


THE  NODAL  RHYTHM  325 

showed  extra-systoles.  These  occurred  sometimes  at  rare,  sometimes  at 
frequent  intervals  (Figs.  99,  103  and  104,  Plate  II).  They  were  usually 
ventricular  in  origin,  but  occasionally  nodal  and  auricular.  I  also  noted 
in  1892  that  there  was  a  gallop  rhythm  of  the  heart  when  it  was  regular. 
In  1900  she  began  to  have  attacks  of  '  palpitation  '  of  short  duration,  and 
I  obtained  tracings  of  the  radial  and  jugular  during  one  of  these  attacks, 
and  they  showed  a  transition  of  the  venous  pulse  to  the  ventricular  form 
during  the  attack.  On  October  13,  1903,  she  felt  weak  and  exhausted,  and 
had  a  distressing  fluttering  sensation  within  her  chest,  and  I  found  the 
heart's  action  extremely  irregular.  The  attack  lasted  four  or  five  hours. 
The  tracings  taken  during  the  attack  were  of  the  same  character  as  Fig.  209. 
On  October  19  she  was  again  seized  with  a  similar  attack,  which  lasted 


Fig.  209.     Characteristic  irregularity  on  the  sudden  inception  of  the  nodal  rhythm — 
the  jugular  pulse  is  of  the  ventricular  form.     (Case  12.) 

a  whole  day,  and  the  tracings  in  Fig.  209  convey  a  very  good  idea  of  the 
character  of  the  heart's  irregularity.  The  next  day  the  heart  was  quite 
regular  and  the  jugular  pulse  a  typical  example  of  the  auricular  form. 

On  October  27  the  heart  again  became  very  irregular.  This  attack 
continued  without  intermission  until  November  1.  On  October  29  the 
heart's  action  became  much  slower,  but  the  irregularity  still  persisted,  and 
the  character  of  the  jugular  pulse  showed  a  curious  change  (Figs.  210  and 
211),  viz.,  during  the  ventricular  systole  (the  period  between  the  perpendi- 
cular lines  3  and  6)  there  are  two  waves  a'  and  v,  while  there  is  no  wave 
at  the  normal  time  of  the  auricular  wave.  The  heart  suddenly  reverted 
to  the  normal  rhythm,  and  became  regular  with  a  typical  auricular  venous 
pulse  (Fig.  212). 

The  attacks  gradually  lessened  in  frequency  and  duration  until  June  12, 
1904,  when,  after  a  long  walk  in  the  country,  she  was  seized  with  an  attack 
which  lasted  for  a  fortnight.  A  few  days  before  the  attack  finally  subsided 
the  heart  became  normal  in  its  rhythm  for  a  few  hours.  On  October  16, 
1904,  this  nodal  rhythm  again  started,  and  continued,  with  great  dilatation 
of  the  heart,  dropsy,  ascites,  and  hydrothorax,  until  her  death  on 
March  17,  1905. 


326 


DISEASES  OF  THE  HEART 


In  this  patient  the  remarkable  changes  described  in  §  159  were  seen 
most  typically.  A  few  hours  after  an  attack  the  heart  dilated,  the  liver 
enlarged,  the  face  became  swollen  and  livid.  Immediately  the  normal 
rhythm  was  restored,  the  patient  at  once  felt  relief,  and  in  a  few  hours  all 
the  abnormal  symptoms  disappeared. 


f                  

Tubular                            g 

i'         a!       CL'         <^'  ^      a.'            ^,                3S-6 

xwna^msa^mB. 

^^  ^^'^^^  ^^  "^"^  ^'^^^ '""^ 

Fig.  210.     The  rhythm  is  still  irregular  and  the  jugular  pulse  is  of  the  ventricular  type, 
the  auricular  wave  a'  occurring  during  the  ventricular  systole.     (Case  12.) 

As  this  patient  Uved  close  to  my  house  I  saw  her  very  frequently,  and 
had  the  opportunity  of  watching  the  attacks  begin  and  finish.  Once  when 
taking  a  tracing  the  attack  started,  and  on  several  occasions  the  attacks 
ceased  while  I  was  watching  her.  I  have  accumulated  a  great  number  of 
tracings  taken  at  all  stages. 


Fig.  211.     Shows  the  same  as  Fig.  210  except  that  during  the  long  pause  of  the  ventricle  an 
independent  auricular  wave  {a')  appears,  not  followed  by  a  v  wave.    (Case  12.) 

The  character  of  the  jugular  tracing  showed  invariably  the  typical 
ventricular  venous  pulse  during  the  attack,  and  the  return  to  the  auricular 
jugular  pulse  with  the  cessation  of  the  attack.  There  are  a  few  instructive 
features  in  the  character  of  the  jugular  pulse.  The  heart's  rate  varied  very 
much  during  the  attack.  At  the  beginning  it  was  usually  very  rapid,  then 
it  began  to  get  slower  in  an  irregular  way  ;  at  first  an  occasional  long  diastolic 
pause  would  occur,  followed  by  a  large  ventricular  contraction.  Then  longer 
pauses  sometimes  became  more  frequent,  till  finally  the  heart's  rate  was 
not  much  above  the  normal,  though  it  was  irregular  in  rhythm  (Figs.  210 
and  211).  "V^Tien  the  rate  was  rapid,  sometimes  there  was  scarcely  any 
evidence  in  the  radial  pulse  of  the  ventricular  contraction,  while  the  jugular 


THE  NODAL  RHYTHM 


327 


pulse  showed  well-marked  waves  during  the  intermission  (Fig.  209)  in  the 
radial  pulse.  When  the  heart  was  rapid,  the  wave  v  in  the  jugular  tracing 
was  full  during  the  whole  of  the  ventricular  systole  ;  but  during  slow  action 
of  the  heart — whether  the  slow  beat  was  occasional,  as  in  Fig.  209,  or  con- 
tinuous, as  in  Fig.  210 — the  wave  v  was  divided  into  two  portions  (a'  and  v) 


Fig.  212.  With  the  sudden  reversion  to  the  normal  rhythm  the  heart  becomes  regular 
and  the  jugular  pulse  of  the  normal  auricular  type.  Compare  this  tracing  with  the  three 
preceding.     (Case  12.) 


by  a  deep  depression.  The  explanation  I  suggest  is  that  the  auricular  contrac- 
tion occurred  during  the  ventricular  systole,  but,  being  short,  it  finished  before 
the  ventricular  systole  (as  in  Cushny's  tracing,  Fig.  58),  and  that  the  wave 
a'  in  these  tracings  is  due  to  the  auricular  systole,  and  the  fall  x  is  due  to 
the  auricular  diastole  (probably  the  other  factors  mentioned  in  §  108  assist 


Fig.  213.     Sometimes  when  the  heart  reverted  to  the  normal  rhythm  ventricular  extra- 
systoles  (r')  would  appear.     (Case  12.) 

in  deepening  this  fall).  When  the  heart  beats  rapidly  the  engorgement 
of  the  right  side  is  so  great  that  it  obliterates  the  effect  of  the  auricular 
diastole.  This  explanation  of  a'  is  supported  by  the  fact  that  sometimes 
during  a  long  pause,  when  the  heart  was  acting  slowly  and  irregularly, 
a  wave,  presumably  auricular  in  origin,  would  appear  as  in  Fig.  211. 
When  the  heart  suddenly  reverted  to  the  normal  rhythm,  then  it  was 
sometimes    quite    regular,    as    in    Fig.    212,    or    there    was    an    occasional 


328 


DISEASES  OF  THE  HEART 


extra-systole,  sometimes  of  auricular  origin,  as  in  Fig.  99,  sometimes 
ventricular,  as  in  Fig.  213.  During  the  last  three  months  of  her  life  the 
rate  was  continuously  rapid,  and  though  I  pushed  such  drugs  as  digitalis  and 
strophanthus  no  change  was  produced.  Fig.  214  was  taken  a  month  before 
she  died. 

Report  of  the  post-mortem  examination  of  the  heart  : — 

Arteries. — Left  coronary  chiefly  affected  ;  lumen  narrowed.  Anterior 
interseptal  artery  which  supplies  the  a. -v.  bundle  closed  completely  ;  right 
coronary  affected,  but  to  a  less  degree. 

Orifices  and  Valves. — Valves  not  diseased.  Mitral  orifice  dilated,  tricuspid 
dilated,  inferior  caval  dilated,  aortic  normal. 

Musculature. — Taenia  terminalis  hypertrophied.  A.-v.  node  and  bundle 
large  ;  the  fibres  have  the  appearance  of  being  stretched,  having  lost  their 
stellate  reticular  form  :   applied  closely,  and  rather  longer  than  usual.     The 


IB^^^^BIIWIHiBll 


Fig.  214.     Shows  tlie  character  of  the  persistent  nodal  rhythm  one  month  before  death. 

(Case  12.) 

right  and  left  septal  divisions  are  normal  in  appearance.  The  inter- 
auricular  septum  is  stretched.  The  apical  two-thirds  of  the  left  ventricle 
shows  large  patches  of  fibrosis,  and  the  trabeculae  with  the  Purkinje  system 
are  stretched,  and  certainly  not  healthy — fibrosis  and  atrophy — result  of 
endarteritis. 

Case  13. — Frequent  attacks  of  the  nodal  rhythm,  with  no  serious  ejects,  in 
old  age. 

Male,  born  1827.  Has  suffered  from  frequent  attacks  of  rapid  action 
of  the  heart,  accompanied  by  a  feehng  of  great  prostration  since  he  was 
seventy-six  years  of  age.  During  the  attacks  he  feels  very  exhausted, 
and  lies  in  bed  ;  they  last  from  half  an  hour  to  twelve  hours.  He  may 
be  free  from  them  for  weeks,  at  other  times  he  has  several  in  one  week. 
I  have  seen  him  in  consultation  during  these  attacks  and  also  when  quite 
free  from  them.  In  the  latter  condition  he  is  a  hale  man,  considering  his 
years,  and  takes  an  active  part  in  his  business  ;  his  heart  shows  no  abnor- 
mality, and  his  pulse  is  slow  and  regular  (Fig.  215).  During  the  attack  he 
lies  very  still  in  bed  ;   his  face  is  pale  and  slightly  drawn.     He  does  not  care 


THE  NODAL  RHYTHM 


329 


to  make  much  exertion,  but  has  no  actual  suffering.  The  pulse  sometimes 
attains  a  rate  of  200  per  minute  at  the  beginning  of  the  attack.  It  was 
always  several  hours  after  an  attack  had  begun  before  I  saw  him,  and  the 
pulse  was  usually  between  150  and  170  beats  per  minute.  Fig.  215  is 
a  tracing  of  his  jugular  and  radial  pulses  while  free  from  the  attack  ;  there 
was  very  slight  pulsation  in  the  neck,  and  I  had  some  difficulty  in  getting 


Fig.  215.     Tracings  from  a  man  aged  78,  when  free  from  an  attack  of  paroxysmal 

tachycardia.     (Case  13.) 

a  tracing.  Its  character,  however,  clearly  shows  it  to  be  of  the  auricular 
form.  Fig.  216  shows  the  radial  and  jugular  pulses  during  an  attack. 
I  had  considerable  difficulty  in  getting  satisfactory  tracings,  as  the  patient 
was  in  bed  in  a  position  not  conducive  to  taking  a  good  tracing,  but  in 
all  those  I  took  the  characters  were  the  same  as  in  Fig.  216.     Here  the 


boranstasiisifHil 

IffiBBBBBml 

JH 

Fig.  216.     From  the  same  patient  that  gave  Fig.  215,  during  an  attack  of  paroxysmal 
tachycardia.     Note  slight  pulsus  alternans  in  the  radial  tracing.     (Case  13.) 

jugular  pulse  is  manifestly  of  the  ventricular  type.  In  the  radial  pulse  there 
is  seen  a  tendency  to  the  alternans  form. 

When  last  I  heard  of  him  (1908),  at  the  age  of  eighty-one,  he  was  in  fair 
health,  and  still  liable  to  these  attacks. 

Case  14. — Attacks  of  paroxysmal  tachycardia. 

Male,  aged  thirty.  Came  under  my  care  suffering  from  a  hydatid  cyst  of 
the  liver.  There  was  no  history  of  any  heart  trouble,  except  that  for  the 
last  two  years  he  had  been  conscious  of  a  rapid  '  fluttering  '  action  of  the 


330 


DISEASES  OF  THE  HEART 


heart.  I  was  about  to  operate  on  him  when  I  felt  his  pulse — it  was  beating 
at  the  rate  of  about  200  beats  per  minute.  He  was  conscious  of  this  rapid 
action,  and  said  that  it  had  come  on  two  hours  previously  when  at  the 
closet.  The  attack  ceased  quite  suddenly  two  hours  afterwards.  I  lost 
sight  of  him  some  months  afterwards,  but  he  seemed  in  no  way  impaired 
by  these  attacks. 

Fig.  217  is  a  tracing  of  the  jugular  pulse  when  he  was  at  rest.  It  is 
a  typical  instance  of  the  auricular  form  of  the  venous  pulse.  Fig.  218  shows 
the  character  of  the  jugular  and  radial  pulses  during  the  attack.  The 
jugular  pulse  is  now  of  the  ventricular  t3rpe. 


Fig.  217.  Simultaneous  tracings  of  the  jugular  ani  radial  pulses  from  a  case  of  paroxysmal 
tachycardia  during  the  quiet  period  of  the  heart's  action.  There  is  a  well-marked  auricular 
wave,  a,  in  the  jugular  pulse.     (Case  14.) 


Fig.  218.  Simultaneous  tracings  of  the  radial  and  jugular  pulses  during  an  attack  of 
paroxysmal  tachycardia.  The  jugular  pulse  is  due  to  the  ventricular  systole,  there  being  now 
no  trace  of  the  amicular  waves.     (From  the  same  patient  as  Fig.  217.     Case  14.) 


Case  15. — Sudden  inceptioyi  of  the  nodal  rhythm,  with  'persistent  rapid 
heart  action,  dilatation  of  the  heart,  dropsy,  death  in  three  weeks. 

Female,  aged  sixty-five.  I  had  attended  her  for  various  ailments 
(rheumatism,  bronchitis,  &c.)  during  a  period  of  over  twenty  years,  and  her 
heart  had  invariably  been  quite  regular.  On  June  20,  1904,  she  returned 
from  the  seaside  to  her  home  and  sent  for  me.  She  had  been  taken  ill 
a  few  days  before,  her  chief  complaint  being  shortness  of  breath.  When 
I  saw  her  she  was  propped  up  in  bed,  and  breathing  rapidly  and  laboriously. 
Her  pulse  was  extremely  rapid  and  irregular,  but  I  did  not  have  my  poly- 
graph with  me.  Next  day  when  I  called  to  see  her,  I  found  her  greatly 
improved,  out  of  bed,  and  free  from  distress.     Her  pulse  was  full,  regular, 


THE  NODAL  RHYTHM 


331 


and  not  rapid  (Fig.  219).  The  following  day,  however,  she  was  again  very 
bad,  and  Fig.  220,  taken  on  June  23,  gives  a  good  idea  of  her  pulse.  She  was 
very  stout  and  short-necked,  and  I  had  difficulty  in  getting  a  jugular  tracing  ; 
her  breatliing  was  laboured  and,  the  sterno-mastoid  being  in  action,  I  could 
only  get  an  imperfect  tracing  from  the  jugular,  as  in  Fig.  220.  Imperfect 
as  it  is,  it  shows  clearly  that  the  venous  pulse  is  of  the  ventricular  form. 
I  tried  all  sorts  of  remedies  to  slow  the  heart — digitahs  and  opium,  adi'enaUn, 
trinitrin,  &c.,  but  all  without  avail.  The  heart  dilated,  di'opsy  set  in  and 
became  very  extensive,  and  she  died  three  weeks  after  the  permanent 
establishment  of  the  nodal  rhythm. 


Fig.  219.     Regular  pulse  between  attacks  of  nodal  rhythm.     (Case  15.) 


Fig.  220.     Permanent  inception  of  nodal  rhythm,  leading  to  a  fatal  issue  in  three  weeks. 

(Case  15.) 

Case  16. — Frequent  attacks  of  paroxysinal  tachycardia  without  serious 
symptoms. 

Female,  aged  thirty-five,  eight  months  pregnant  with  her  second  child. 
For  several  years  she  suffered  from  breathlessness,  and  was  conscious  that 
her  heart  beat  '  very  queerly  '.  She  was  under  my  care  for  only  a  few  weeks, 
and  I  saw  her  during  several  attacks  of  paroxysmal  tachycardia.  After  she 
left  me  I  heard  that  she  had  had  an  easy  confinement,  and  some  years  later 
was  in  fair  health,  though  still  at  times  prostrate  on  account  of  her  heart. 
The  periods  of  nodal  rhythm  were  of  varying  duration,  the  attacks  not  being 
continuous,  but  interrupted  frequently  by  normal  beats.  At  other  times 
the  heart  would  only  show  frequent  extra-systoles.  When  the  heart  was 
irregular  the  venous  pulse  was  always  large,  while  when  the  heart  was  regular 


332 


DISEASES  OF  THE  HEART 


it  was  scarcely  perceptible,  and  it  was  with  difficulty  that  I  got  the  faint 
tracing  of  it  in  Fig.  221.  The  waves  in  the  jugular,  though  slight,  are  recog- 
nizable, and  the  jugular  pulse  is  of  the  auricular  type.  In  Fig.  222  the  heart 
is  acting  irregularly.  The  radial  pulse  shows  three  long  pauses  at  x  x  X . 
The  auricular  waves,  a  and  a\  in  the  venous  pulse  occur  at  regular  intervals. 
During  each  long  pause  in  the  radial  there  is  a  large  wave,  a',  due  to  the 
auricle,  and  larger  than  the  other  auricular  waves,  for  the  reason  already 
given,  p.  153,  namely,  because  at  the  period  at  which  the  auricle  contracted 


\^i  Jugular  «,, 


i 


RctdxcLl     ' 


Fig.  221.  Simultaneous  tracings  of  the  jugular  and  radial  pulses.  The  jugular  pulse 
is  of  the  auricular  form.  These  and  the  following  four  tracings  are  from  the  same  patient. 
(Case  16.) 


Fig.  222,  Simultaneous  tracings  of  the  jugular  and  radial  pulses  during  irregular  action 
of  the  heart.  The  auricle  preserves  its  rhythm,  there  being  a  large  wave,  a',  during  the  pre- 
mature contraction  of  the  ventricles.     (Case  16.) 


Fig.  223.     Shows  the  same  as  Fig.  222.     (Case  Iti.) 

the  ventricle  was  in  systole,  and  hence  a  larger  wave  was  sent  back  into 
the  veins.  It  wiU  be  noted  that  after  the  large  auricular  wave,  a',  there 
is  never  a  ventricular  wave.  This  tracing  exemplifies  the  form  of  irregu- 
larity due  to  premature  stimulation  of  the  ventricles  alone  .(ventricular 
extra-systole). 

In  Fig.  223  a  very  similar  irregular  condition  is  present,  the  difference 
being  that  every  third  arterial  beat  here  is  missed,  and  is  represented  in 
the  radial  tracing  by  the  notch  n' .  In  these  three  tracings  (Figs.  221, 
222,  and  223)  the  period  E,  representing  the  time  when  the  semilunar  valves 


THE  NODAL  RHYTHM 


333 


are  open,  shows  in  the  jugular  pulse  a  great  fall.  In  Fig.  224  the  radial 
tracing  shows  two  normal  beats  in  the  centre  of  the  tracing,  all  the  others 
being  nodal  in  origin.  The  beat  preceding  the  full  beats  shows  only  a 
notch,  n',  as  in  Fig.  222.  The  venous  pulse  at  the  time  of  the  normal 
radial  beats  shows  the  same  features  as  are  present  with  the  normal  radial 
beats  in  the  three  preceding  tracings,  namely,  a  small  auricular  wave,  a, 
the  carotid  wave  c,  the  auricular  depression  during  the  period  E,  and  the 
ventricular  wave   v.      But  when   the  venous  pulse   corresponding  to  the 


Fig.  224.  Simultaneous  tracings  of  the  jugular  and  radial  pulses,  showing  two  norma 
radial  beats  in  the  centre  of  the  tracing.  Coriespondirg  to  the  ventiicular  systole,  E,  there  is 
a  fall  in  the  jugular  pulse  when  the  radial  beat  is  normal,  and  a  rise,  E',  when  it  is  of  nodal 
origin.     (Case  16.) 


Fig.  225.     Shows  an  alternation  of  the  normal  and  nodal  rhythms.     (Case  16.) 


E 

e'         Rad. 

^"^■-^wv^ 

^^r^  -^V.JV-'V-AyJV.A.-JVvA^-^^^' 

AAx— ih^ 

^\r- 

v^VvvwvvVaa./- 

E 

e'          -^^ff- 

Fig.  226.     There  is  only  one  normal  beat  {E),  all  the  other  beats  being  of  noda 

origin.     (Case  16.) 

nodal  beats  is  considered,  a  remarkable  change  is  found.  There  is 
but  one  large  wave  and  one  large  fall,  and  the  period  when  this  wave  occurs  is 
during  the  ventricular  systole  E',  in  striking  contrast  to  the  large  depression  at 
the  time  with  the  normal  radial  beats  showTi  in  the  preceding  three  tracings. 
A  similar  condition  is  seen  in  Fig.  225,  where  there  is  a  continuous  variation 
from  the  normal  rhythm  to  the  nodal.  In  Fig.  226,  with  the  exception  of 
one  normal  beat  preceded  by  a  long  pause,  the  jugular  pulse  is  of  the  ven- 
tricular form.  The  transition  from  one  form  of  jugular  pulse  to  the  other 
is  well  brought  out  in  Fig.  225. 


APPENDIX   III 

Paroxysmal  Tachycardia  of  Auricular  Origin 

In  reflecting  upon  the  causes  of  abnormal  rhythms  of  the  hearty  it  seemed 
reasonable  to  expect  that  at  the  place  where  an  occasional  stimulus  arose 
giving  rise  to  an  extra-systole  it  would  be  probable  that  the  same  place 
might  start  off  the  heart's  action  continuously.  This  view  has  been  con- 
firmed in  the  instances  of  ventricular  and  nodal  extra-systoles  being  the 
precursors  of  the  nodal  rhythm.  I  had  considered  that  inasmuch  as  auricular 
extra-systoles  were  of  frequent  occurrence,  it  would  be  but  reasonable  to 
expect  that  the  heart's  action  might  in  some  cases  start  continuously  from 
the  place  at  which  the  auricular  extra-systoles  arose.  In  preparing  the 
first  edition  of  this  book  I  had  examined  my  records  for  such  a  condition 
and  found  a  number  of  cases  that  seemed  to  fulfil  this  prediction.  In  four 
instances  the  patients  were  suddenly  seized  with  great  rapidity  of  the 
heart's  action,  and  they  all  died  from  heart  failure  after  a  period  varying 
from  one  to  four  weeks.  The  tracings  taken  from  these  patients  present 
considerable  difficulty  in  their  interpretation,  but  I  could  only  conclude 
that  they  were  cases  of  auricular  tachycardia.  In  two  other  cases  there 
seemed  distinct  evidence  of  a  paroxysmal  tachycardia  of  auricular  origin. 
As  the  tracings  were  not  altogether  convincing  I  did  not  allude  to  the 
matter,  but  resolved  to  wait  for  further  experience.  Within  the  past  year 
cases  of  undoubted  paroxysmal  tachycardia  have  been  published  by 
Cowan,  Macdonald  and  Binning  ^^s^  and  Lewis  ^^i,  while  a  case  of  continuous 
auricular  tachycardia  has  been  published  by  Hertz  and  Goodhart  ^43^  and 
Dr.  W.  T.  Ritchie  has  shown  me  another. 

I  have  at  present  under  observation  a  very  instructive  case  of  this 
auricular  form  of  paroxysmal  tachycardia.  The  patient,  a  man  aged  41, 
a  carpenter  by  trade,  complains  of  weakness,  palpitation,  and  attacks  of 
giddiness.  The  radial  pulse  is  soft  and  compressible,  and  shows  a  varied 
irregularity.  At  times  there  may  be  an  occasional  intermission,  or  these 
intermissions  may  be  very  frequent.  At  irregular  intervals  the  rate  becomes 
suddenly  very  rapid,   and  as  suddenly  becomes  slow.     These  periods  of 


PAROXYSMAL  TACHYCARDIA  OF  AURICULAR  ORIGIN    335 

rapid  action  may  last  for  a  few  seconds  or  for  ten  minutes.  Tracings 
taken  of  the  radial  and  jugular  pulses  show  the  intermission  to  be  due, 
as  a  rule,  to  auricular  extra-systoles,  when  the  ventricle  failed  to  respond 


Fig.  227.  Simultaneous  tracings  of  the  jugular  and  radial  pulses  during  one  attack  of 
paroxysmal  tachycardia.  The  first  cardiac  cycle  in  the  jugular  tracing  shows  the  normal 
events  {a,  c,  v).  The  second  cycle  shows  the  normal  waves  a  and  c,  but  the  wave  following 
marked  a'  occurs  earlier  than  the  wave  v  in  the  previous  cycle,  and  is  due  to  a  premature 
or  auricular  extra-systole,  but  is  not  followed  by  a  c  wave  or  by  a  radial  pulse  beat.  The 
next  two  normal  a,  c,  waves  are  each  followed  by  an  auricular  extra-systole  (a')  with  no 
ventricular  response,  as  shown  by  the  absence  of  the  c  wave  and  the  radial  pulse  beat.  These 
are  all  '  interpolated  auricular  extra-systoles  '.  After  these  there  follows  a  series  of  auricular 
premature  beats  (a')  to  which  the  ventricle  responds  as  shown  by  the  c  waves  and  the  small 
radial  puis  3  beats. 

The  onset  of  the  paroxysm  always  coincides  with  great  distension  of  the  jugular  veins, 
which  is  shown  in  the  tracing  by  the  greater  amplitude  of  the  auricular  waves  a'. 


r    r    Q.    a'    A      k     a    ^.     ^    a'  ^'    9'    a' 


Fig.  228.  From  the  same  patient  as  Fig.  227,  taken  at  the  end  of  a  long  paroxysm.  It 
shows  the  same  features  as  Fig.  227,  but  here  there  is  a  well-marked  alternation  of  the  radial 
pulse  beats  during  the  paroxysm. 

to  the  auricular  extra-stimulus,  or  responded  so  weakly  that  the  pulse  beat 
did  not  reach  the  radial  (Figs.  227  and  228). 

The  rapid  pulse  beats  in  the  radial  are  seen  to  be  in  response  to  a 
rapid  series  of  auricular  contractions — the  waves  a'  in  Figs.  227  and  228 


336  DISEASES  OF  THE  HEART 

being  due  to  the  abnormal  series  of  auricular  contractions.  In  Fig.  227 
one  of  these  short  paroxysms  is  shown,  while  in  Fig.  228  there  is  shown 
the  end  portion  of  a  long  attack.  The  radial  pulse  shows  a  well- 
marked  pulsus  alternans,  a  feature  not  infrequently^  found  after  a  long 
paroxysm  in  the  more  common  form  of  nodal  paroxysmal  tachycardia 
(see  Fig.  130,  p.  198). 


APPENDIX    IV 

Nodal  Bradycardia 

I  HAVE  already  remarked  that  in  the  vast  majority  of  cases,  where  the 
nodal  rhythm  is  present,  the  heart's  action  is  at  first  more  rapid  than  normal, 
but  there  is  a  class  of  case  where,  so  far  from  the  rate  of  the  contraction 
being  more  rapid  than  the  normal,  it  becomes  slower,  and  sometimes  very 
markedly  so.  In  most  other  respects  the  character  of  the  heart's  action 
corresponds  to  the  more  common  forms  of  nodal  rhythm,  but  if,  as  seems 
probable,  these  commoner  forms  owe  their  inception  to  disease  rendering 
some  part  of  the  heart,  such  as  the  node,  more  excitable,  this  cannot  hold 
good  when  the  rate  is  much  slower  than  that  of  the  normal  rhythmic  area. 
Hence  a  search  has  to  be  made  for  some  other  cause.  Facts  pointing  to 
a  definite  cause  may  appear  when  all  the  features  connected  with  these 
cases  are  studied,  and  are  compared  with  the  results  of  experiment.  There 
is  probably  more  than  one  form  of  this  nodal  bradycardia,  for,  in  the  cases 
I  have  collected,  in  some  the  pulse  though  slow  is  quite  regular,  while  in  others 
it  is  continuously  irregular. 

In  some  of  these  cases  the  heart's  action  becomes  so  slow  that  cerebral 
anaemia  results,  with  all  the  phenomena  characteristic  of  the  Adams-Stokes 
syndrome,  so  that  they  may  easily  be  mistaken  for  heart-block.  The 
differential  diagnosis  between  cases  of  nodal  rhythm  and  heart-block  lies  in 
this — in  heart-block  the  auricle  is  active  and  independent  of  the  ventricular 
systole,  so  that  there  is  never  a  jugular  pulse  of  the  ventricular  form  ;  the 
ventricular  form  of  the  venous  pulse,  on  the  other  hand,  is  characteristic  of 
the  nodal  bradycardia. 

Case  17. — Old  rheumatic  affection  of  the  heart,  with  long-continued  impair- 
ment of  the  a.-v.  bundle,  with  a  delay  between  the  As  and  Vs.  Sudden  inception 
of  a  slow  and  irregular  action  of  the  heart,  with  disappearance  of  all  evidences 
of  auricular  contraction,  at  first  transient,  later  permanent. 

Male,  born  in  1851.  I  attended  him  for  an  attack  of  rheumatic  fever  in 
1883.  He  was  left  with  a  damaged  mitral  valve,  but  remained  in  fair  health 
till  1897,  when  he  had  serious  heart  failure.  From  this  also  he  made  a  good 
recovery,  and  his  heart  remained  perfectly  regular  till  1904.  I  have  taken 
tracings  of  his  apex,  radial  pulse,  and  jugular  pulse  at  frequent  intervals 

MACKENZIE  •/, 


338 


DISEASES  OF  THE  HEART 


since  1892,  His  heart  was  invariably  regular  except  for  a  short  period  in 
1897,  the  irregularity  being  due  to  dropping  out  of  ventricular  systoles 
<mild  heart-block,  see  Fig.  115).  His  jugular  pulse  was  always  of  the 
auricular  form,  a  peculiarity  in  this  case  being  a  persistent  increase  in  the 
a-c  interval.  Tracings  of  the  jugular  and  radial  pulses,  taken  in  1892,  are 
given  in  Fig.   229  ;    in   1903  in  Fig.   230.     Jugular  and  apex  tracings  are 


i 

A «        } 

h/V 

mmmmum 

/Radial 

2,Ur 

r^''^           -w        -— ^ 

Fig.  229.     Shows  a  regular  rhythm  and  an  auricular  venous  pulse  and  wdde  a-c  interval 
(space  A).     Taken  1892.     (Case  17.) 

represented  in  Fig.  231.  The  rhythm  is  regular,  and  the  auricular  wave, 
a,  is  well  marked  in  both  apex  and  jugular  tracings.  There  was  a  long 
diminuendo  murmur  after  the  second  sound,  and  a  well-marked  presystolic 
murmur  separated  by  a  brief  interval  from  the  first  sound   (shading  in 


Fig.  230.     Shows  a  regular  rhythm  and  an  auricular  venous  pulse  and  wide  a-c  interval 
(space  A).     Taken  1903.     (Case  17.)     (Figs.  229  and  230  are  also  discussed  in  §  164.) 

Fig.  230).  In  the  numerous  tracings  of  the  apex  beat  I  have  taken  up  to 
April  19,  1904,  there  was  always  a  well-marked  auricular  wave,  a,  preceding 
the  large  wave.  When  he  visited  me  on  the  last-named  date  I  found  his 
heart  continuously  irregular,  and  on  taking  tracings  of  the  jugular  pulse 
I  found  it  of  the  ventricular  type  (Figs.  232  and  233),  the  presystolic  murmur 
had  gone,  and  there  was  at  the  time  only  a  diastolic  murmur  as  shaded  in 
Fig.  232.     The  wave  due  to  the  auricular  systole  had  disappeared  from  the 


NODAL  BRADYCARDIA 


339 


apex  tracing.  Here,  again,  with  the  appearance  of  the  ventricular  venous 
pulse  and  continuous  irregularity  all  evidences  of  the  contraction  of  the 
right  and  left  auricles  had  disappeared.     When  this  patient  called  to  see  me 


Fig.  231.  Shows  the  auricular  wave  (a)  in  jugular  and  apex  tracings.  There  is  an  increase 
in  the  time  from  the  beginning  of  the  auricular  wave  (a)  to  the  large  wave  due  to  the  ventricle 
in  the  apex  tracing,  and  a  corresponding  increase  in  tlie  a-c  interval  in  the  jugular  tracing. 
Taken  1903.     (Case  17.) 


Fig.  232.  With  the  inception  of  the  nodal  rhythm  the  heart  is  irregular,  the  auricular 
wave  is  gone  from  jugular  and  apex  tracings  (compare  with  Fig.  231),  and  the  shading 
underneath  shows  a  disappearance  of  the  presystoUc  murmur.     (Case  17,  April  19,  1904.) 


in  the  following  week  I  found  his  heart  perfectly  regular,  the  auricular  wave 
present  in  the  venous  pulse,  the  presystolic  murmur,  and  the  auricular  wave 
in  the  apex  tracing  also  present  (Fig.  234).      These  conditions  continued 

z  2 


340  DISEASES  OF  THE  HEART 

until  November,  1904,  when  his  heart  again  became  irregular,  and  all 
evidence  of  auricular  systole  again  disappeared.  From  that  date  up  to  the 
present  (1908)  the  heart  has  remained  in  this  state,  and  on  the  numerous 
occasions  when  I  have  taken  long  tracings  I  have  never  yet  found  the  heart 
regular  for  one  moment  (Fig.  238,  Plate  III). 


Fig.  233.     Shows  a  slow  irregular  rhythm  with  the  ventricular  form  of  the  venous  pulse. 

(Case  17,  April  19,  1904.) 


Fig.  234.     Shows  a  regular  rhythm  and  the  presence  of  the  auricular  wave  in  the  apex  and 
jugular  tracings.     (Case  17,  April  26,  1904.) 

Case  18. — Sudden  inceptio?i  of  nodal  bradycardia,  lasting  for  about  three 
weeks. 

Male,  born  1852,  a  stout,  healthy-looking  individual.  I  had  known  him 
for  about  twenty-eight  years,  and  had  attended  him  at  various  times  for 
trivial  complaints,  and  in  1903  for  an  attack  of  erysipelas  of  the  face.  He 
had  enjoyed  good  health,  was  getting  fat  and  somewhat  short  of  breath. 
On  November  9,  he  was  hurrying  from  the  train  to  a  football  match,  a  mile 
distant  from  the  station.  As  he  approached  the  football  field  he  was  seized 
with  pain  across  the  middle  of  the  chest,  but  as  it  was  not  severe  he  pushed 
on  tiU  he  arrived  at  the  field.  He  sat  down,  but  the  pain  increased,  striking 
into  both  arms,  and  his  hands  went  white  and  cold.  He  felt  as  if  he  wanted 
to  breathe  deeply  but  could  not.  He  endured  the  suffering  for  twenty 
minutes,  and  as  it  became  worse,  and  he  felt  as  if  he  would  die,  he  was 
assisted  'off  the  field,  put  into  a  cab  and  driven  to  the  station.     He  was 


NODAL  BRADYCARDIA 


341 


given  some  brandy,  which  made  him  sick.  The  pain  gradually  diminished, 
and  he  returned  home  by  train  ;  as  he  was  better  he  walked  home  (about 
a  quarter  of  a  mile),  but  felt  sick  and  short  of  breath.  He  went  to  bed, 
and  one  of  my  colleagues  saw  him  and  found  his  pulse  between  30  and 
40  beats  per  minute.  I  saw  him  next  morning.  He  felt  very  weak  ;  the 
pain  was  nearly  gone,  though  it  had  kept  recurring  through  the  night.  He 
had  some  pain  if  he  took  a  deep  breath.  The  pulse  rate  was  52,  the  heart's 
dullness  extended  from  mid-sternum  to  2  inches  beyond  the  nipple  line  ; 
apex  beat  faint  in  the  fifth  interspace  ;  sounds  clear  and  free  from  murmur. 
The  superficial  jugular  vein  was  very  full,  but  did  not  pulsate.  The  deep 
jugular  was  large,  filling  up  during  ventricular  systole,  and  collapsing 
suddenly  at  the  beginning  of  ventricular  diastole.  There  was  no  sign  of 
an  auricular  wave  preceding  the  ventricular  systole.     The  patient  was  kept  in 


fn-y^t.  /y^fj-- 


FiG.  235.  Simultaneous  tracings  of  the  jugular  and  radial  pulses.  The  jugular  pulse  is 
of  the  ventricular  form,  and  shows  the  wave  a'  preceding  by  a  short  interval  the  time  of  the 
carotid  pulse  (perpendicular  line  3).     Pulse-rate,  40  per  minute.     (T.A.,  November  24,  1907.) 


bed,  and  his  condition  did  not  undergo  much  change  for  the  next  fortnight, 
except  that  the  pain  gradually  grew  less  till  it  finally  disappeared  and 
he  was  able  to  sit  up.  The  pulse-rate  varied,  sometimes  falling  as  low 
as  30,  but  never  rising  above  52.  On  November  24  a  long  tracing  was 
taken  with  the  ink  polygraph,  and  the  rate  showed  great  uniformity  ;  the 
rhythm  was  also  quite  regular.  Fig.  235  is  a  small  portion  of  the  tracing 
taken  on  that  day,  and  represents  the  same  features  as  were  present  on 
November  10  ;  the  rate  was  40  per  minute,  the  rhythm  regular,  and  the 
venous  pulse  of  the  ventricular  form.  When  I  next  examined  him  on 
November  29,  his  pulse  had  increased  in  rate,  with  occasional  intermissions. 
I  had  the  greatest  difficulty  in  getting  a  tracing  of  the  jugular  pulse  ;  he 
had  a  very  short  fat  neck.  But  imperfect  as  the  tracings  were,  they  showed 
a  return  of  the  auricular  wave  a  to  its  normal  period  before  c.  From  this 
date  he  gradually  improved,  and  has  been  able  to  get  about,  though  he  is 
perhaps  a  little  shorter  of  breath  than  before  his  attack.  Tracings  were 
taken  from  him  in  December,   1908,  and  on  May  11,   1909.     The  venous 


342  DISEASES  OF  THE  HEART 

pulse  was  the  same  on  both  occasions,  and  showed  an  auricular  wave,  a, 
preceding  the  carotid  wave,  c,  while  the  rate  was  68  per  minute  ;  the 
rhythm  was  regular. 

Case  19. — Inceptioii  of  the  nodal  rhythm,  the  heart's  rate  at  first  not 
infrequent,  but  becoming  slow  with  attacks  of  unconsciousness  and  epileptic 
fits.    Recovery  from  these  attacks  with  an  increase  in  the  heart's  rate. 

Male,  born  1838.  I  have  known  this  patient  intimately  since  1894. 
He  was  a  healthy,  vigorous  man  up  till  1907.  He  was  a  very  heavy  smoker, 
and  for  a  great  many  years  he  smoked  two  ounces  of  tobacco  and  half 
a  dozen  cigars  a  day.  I  had  occasion  to  examine  him  in  1906,  and  found 
his  heart  normal  in  rate  and  rhythm,  though  for  some  years  he  had  been 
rather  short  of  breath.  I  again  examined  him  in  February,  1907,  and 
found  that  his  heart  was  continuously  irregular  mth  the  disorderly  rhythm 
characteristic  of  the  nodal  rhythm.  He  was  not  conscious  of  the  change, 
but  there  was  a  further  increase  in  his  breathlessness.  He  was  still  able 
to  attend  to  business,  and  to  play  a  game  of  goH.  He  Uved  some  distance 
from  me,  and  I  did  not  see  him  again  until  October  11,  1907,  when  I  was 
asked  to  see  him  with  his  medical  attendant,  Dr.  O'Connor,  to  whom  I  am 
indebted  for  an  excellent  account  of  his  many  seizures.  The  history  given 
was  that  his  pulse  had  become  very  slow  for  some  months,  and  that  latterly 
he  had  been  seized  at  times  with  attacks  of  unconsciousness.  The  pulse- 
rate  on  such  occasions  was  found  below  30  beats  per  minute.  He  was  very 
weak  and  faint  when  I  saw  him,  the  pulse  varying  in  rate  from  30  to  40 
beats  per  minute,  and  irregular  with  long  pauses  at  times.  During  the 
long  pauses  there  was  often  a  small  premature  beat  in  the  jugular  (see 
v' ,  Fig.  236).  The  heart's  dullness  extended  1|  inches  beyond  the  left  nipple, 
and  there  was  a  soft  blowing  murmur  at  the  apex.  There  was  a  small 
amount  of  albumen  in  the  urine.  The  attacks  of  unconsciousness  continued, 
and  I  saw  him  again  in  November,  when  the  heart's  condition  was  much 
the  same.  After  this  the  pulse-rate  increased,  the  attacks  disappeared, 
and  he  went  to  Torquay  in  June,  1908,  where  he  had  a  slight  recurrence 
of  his  attacks  of  loss  of  consciousness.  From  this  he  recovered,  and  con- 
tinued well  till  August  4,  when  after  some  effort  he  was  seized  with  great 
breathlessness,  and  the  attacks  of  unconsciousness  recurred.  These  increased 
in  number  and  severity,  and  for  two  whole  days  he  was  unconscious  and 
deeply  cyanosed.  ^  For  some  hours  he  passed  from  one  epileptic  seizure  to 
another  as  if  affected  with  uraemic  convulsions.  He  also  developed  Cheyne- 
Stokes  respiration.  The  pulse  during  these  convulsive  attacks  was  not 
perceptible.  The  severity  of  the  attacks  gradually  lessened,  and  in  the 
month  of  September  his  pulse-rate  rose  to  50  or  60  beats  per  minute.     In 


NODAL  BRADYCARDIA  343 

October  he  had  a  number  of  very  transient  fainting  attacks.  Dr.  O'Connor 
described  the  attacks  as  resembling  petit  mal.  Thus,  while  the  doctor 
was  talking  to  him,  the  patient's  face  would  suddenly  become  pale,  and 
consciousness  would  be  lost  for  a  brief  period.  During  these  attacks  no 
pidse  could  be  felt  at  the  radial. 

I  saw  him  again  on  December  18,  1908.  He  was  able  to  go  about, 
and  had  been  free  from  attacks  for  a  few  weeks.  The  pulse  was  rather 
slow,  about  60  per  minute,  and  irregular.  The  heart's  dullness  extended 
1|  inches  beyond  the  left  nipple,  the  sounds  were  clear,  with  a  faint  doubling 
of  the  first  sound.  There  was  no  dropsy,  and  the  urine  was  free  from 
albumen. 

On  May  5,  1909,  he  was  seen  by  Dr.  John  Hay,  who  took  a  long  tracing 
with  the  ink  polygraph.     The  rhythm  was  of  the  disorderly  kind,  charac- 


FiG.  236.  Simultaneous  tracings  of  the  jugular  and  radial  pulses.  The  jugular  pulse  is 
of  the  ventricular  form.  During  the  long  pauses  in  the  radial  pulse,  there  are  small  premature 
beats,  v',  in  the  jugular.  The  pulse-rate  varied  from  25  to  30  beats  per  minute.  The  patient 
was  just  recovering  from  a  series  of  syncopal  and  epileptic  attacks.    (W.N.,  October  11,  1907.) 


teristic  of  the  nodal  rhythm,  and  the  jugular  pulse  was  of  the  ventricular 
form.  In  August,  1909,  the  heart's  action  became  very  infrequent,  and  he 
was  seized  with  attacks  of  loss  of  consciousness  and  epileptic  convulsions,  and 
he  died  in  one  of  these  attacks. 

I  had  looked  upon  this  case,  at  first,  as  an  instance  of  Adams-Stokes 
syndrome,  due  to  heart-block,  but  at  the  time  I  was  puzzled  to  account  for 
the  fact  that  he  had  nodal  rhythm  prior  to  the  onset  of  the  attacks  of  uncon- 
sciousness and  slow  heart-rate,  and  also  because  of  the  nature  of  the  jugular 
pulse,  which  was  of  the  ventricular  type.  The  tracing  of  the  jugular  has  never 
been  shown  to  be  of  this  type  in  cases  of  heart-block.  Case  18,  which  came 
under  my  observation  in  December,  1907,  also  puzzled  me,  and  it  was  only 
when  I  began  to  analyse  the  tracings  more  carefully  that  the  nature  of  the 
tracings  from  this  patient  dawned  upon  me,  and  that  it  became  obvious  that 
here  we  had  an  instance  not  of  blocking  of  the  stimulus  between  auricle  and 
ventricle,  but  one  of  slow  nodal  rhythm  producing  anaemia  of  the  brain. 


344  DISEASES  OF  THE  HEART 

Case  20. — Permanent  nodal  rhythm,  bradycardia  associated  ivith  mitral 
stenosis.  Occasional  attacks  of  syncope  and  convulsions  {Adams-Stokes 
syndrome). 

Male,  born  1865.  When  a  soldier  in  India  he  had  dysentery  at  the  age 
of  20,  syphilis  at  the  age  of  22.  He  had  malarial  fever  in  America  at  the 
age  of  27.  In  1894  he  had  the  first  attack  of  syncope.  After  lying  up 
a  week  he  went  out,  and  in  hurrying  to  avoid  a  cab  he  fell  unconscious 
on  the  pavement,  but  quickly  recovered.  He  consulted  a  doctor,  who  said 
his  heart  was  affected.  Two  years  later  he  was  laid  up  with  shortness  of 
breath  and  swelling  of  the  legs,  and  was  treated  for  '  mitral  disease  '.  He 
partially  recovered,  and  had  frequent  attacks  of  weakness  until  the  final 


Fig.  237.     Simultaneous  tracings  of  the  jugular  and  radial  pulses.     The  jugular  pulse  is  of 
the  ventricular  form,  and  the  rate  about  28  per  minute.     (M.M.,  November  9,  1908.) 

breakdown  occurred  in  1905.  He  had  been  feeling  ill  for  some  years,  but 
had  worked  hard,  and  had  kept  himself  going  on  brandy,  bovril,  eggs,  &c. 
He  says  his  pulse  was  slow  four  years  ago,  and  that  it  has  remained  so  ever 
since. 

In  1904  he  began  to  have  mild  *  fits  '  in  which  he  lost  consciousness 
and  was  slightly  convulsed.  From  November,  1905,  to  April,  1906,  he  had 
a  great  number  of  fits,  some  severe  with  convulsions  and  cyanosis,  others 
slight  without  convulsions.  He  had  no  attacks  for  a  year,  but  he  had 
a  very  severe  one  in  April,  1907,  and  since  then  only  three  mild  attacks. 
He  had  lived  a  life  of  hard  work  with  frequent  bouts  of  drinking. 

The  patient  is  taU,  spare,  and  intelligent  looking.  The  face  is  usually 
ruddy,  with  a  faint  duskiness.  He  walks  slowly  and  carefully,  and  his 
gait  is  slightly  ataxic  ;  if  he  hurries  or  gets  excited  he  becomes  giddy. 
He  has  a  somewhat  violent  temper,  and  when  in  a  passion  his  face  becomes 
dusky  and  cyanosed.  When  lying  down  there  is  a  large  pulsation,  seen 
in  the  deep  jugular  on  both  sides,  heaving  in  the  lower  part  of  the  neck, 
as  in  Fig.  237.     It  is  very  slow  and  synchronous  with  the  apex  beat. 

The  radial  pulse  is  slow  and  deliberate,  usually  about  30  per  minute, 
and  usually  quite  regular.     At  times  two  beats  are  close  together,  and  are 


NODAL  BRADYCARDIA  345 

followed  by  a  long  pause.  These  coupled  beats  may  appear  at  rare  intervals 
or  alternate  with  a  single  beat,  or  they  may  appear  continuously  for  a  short 
period.  The  apex  beat  is  large  and  diffuse  in  the  sixth  interspace,  and  in 
the  anterior  axillary  line.  The  heart  dullness  extends  1  inch  to  the  right 
of  the  middle  hne  and  8  inches  to  the  left. 

There  is  a  rough  blowing  systolic  murmur  heard  best  at  the  apex  and 
propagated  towards  the  axilla.  The  second  sound  is  clear  and  well  struck 
and  followed  by  a  soft  murmur.  This  diastohc  murmur  is  heard  only  over 
a  limited  space  at  the  apex,  and  is  not  always  perceptible.  It  is,  as  a  rule, 
faint  and  fades  away. 

A  large  number  of  tracings  have  been  taken  from  this  patient  at  different 
times  and  they  always  present  the  same  features,  the  only  difference  being 
that  sometimes  the  coupled  beats  are  more  frequent  or  are  entirely  absent. 
The  jugular  tracing  shows  one  large  wave  occupying  the  whole  time  of 
ventricular  systole. 

The  Tendency  to  Standstill  of  the  Heart  in  Nodal 
Rhythm,  with  Notes  of  Two  Cases 

The  tendency  for  long  pauses  in  the  heart's  action  in  cases  of  nodal 
rhythm,  such  as  those  seen  in  Cases  17  and  19,  has  been  a  matter  of  interest 
to  me  for  many  years.  These  pauses  may  not  produce  any  symptoms,  but 
they  may  last  long  enough  to  produce  anaemia  of  the  brain  with  transient 
loss  of  consciousness,  and  even  the  more  prominent  phenomena  of  Adams- 
Stokes  syndrome  (Cases  19  and  20).  The  symptoms  then  resemble  those 
of  the  more  common  condition,  auriculo-ventricular  block.  I  have  been 
impressed  by  the  fact  that  not  a  few  cases  of  nodal  rhythm  die  suddenly, 
and  it  seems  that  this  tendency  to  long  pauses  shown  in  the  figures  may 
be  the  immediate  cause  of  death,  as  in  the  following  case.  The  proof  of 
this  view  is  not  complete,  but  the  following  cases  are  also  very  suggestive. 

Case  21. — Nodal  rhythm,  with  long  pauses  in  the  heart's  action,  producing 
attacks  of  unconsciousness  and  'probably  the  death  of  the  patient. 

Female,  born  1854.  I  had  known  this  lady  for  many  years.  She  had 
a  large  goitre,  and  for  the  last  few  years  of  her  life  her  heart  was  con- 
tinuously irregular.  She  was  not  robust,  but  was  able  to  attend  to  her 
household  duties  ;  she  was  liable  to  attacks  of  palpitation,  and  had  frequent 
attacks  of  syncope,  which  I  could  not  account  for  at  that  time.  On  July  2, 
1902,  I  was  summoned  to  see  her,  and  on  my  arrival  I  found  her  recovering 
from  an  attack  of  unconsciousness  during  which  she  had  been  convulsed. 
Her  face  had  a  deathly  ex-sanguine  appearance.     She  gradually  recovered, 


346  DISEASES  OF  THE  HEART 

and  her  colour  improved  in  the  course  of  half  an  hour.  On  inquiry,  I  found 
that  she  was  talking  to  her  sister  when  she  fell  down  in  a  faint  and  became 
convulsed  for  a  few  minutes. 

When  I  examined  her,  the  heart  was  acting  irregularly  but  with  fair 
strength.  During  the  next  few  days  her  heart  was  irregular  with  long 
pauses,  as  shown  in  Fig.  239,  taken  on  July  3,  1902.     She  sometimes  lost 


Fig.  239.  Simultaneous  tracings  of  the  apex  beat,  and  of  the  radial  pulse.  The  rhythm 
is  disorderly  and  characteristic  of  the  nodal  rhythm,  with  frequent  long  pauses.  It  was 
probably  in  consequence  of  these  long  pauses  that  the  patient  suffered  from  attacks  of 
unconsciousness  and  convulsions.     (M.B.,  July  7,  1902.) 

consciousness  for  a  few  seconds,  but  I  did  not  see  her  at  those  times.  On 
July  7  I  was  again  summoned  to  see  her,  but  when  I  arrived  she  was  dead. 
I  was  informed  that  she  had  again  fainted,  become  convulsed,  and  then 
lay  quite  quiet. 


■■MM^^l^HH^HMHHM^^l^^BHIH^H^I^HHail^^^^^ia^^lMHBHI^HBIi^HBHHa 


Fig.  240.     The  jugular  pulse  shows  a  large  auricular  wave  and  an  increased  a-c  interval 

(space  A).     (Case  22.     1892.) 

Case  22. — Large  auricular  waves  in  the  jugular  and  liver  pulsation.  Pre- 
systolic mitral  and  tricuspid  murmurs.  Auricular  sound  over  the  valves  in  the 
large  veins.  Sudden  disappearance  of  all  signs  of  auricular  contraction,  with 
the  appearance  of  continuous  irregularity  in  the  heart's  action.    Sudden  death. 

Female,  born  1862  ;  came  under  my  care  in  1891.  She  suffered  from 
shortness  of  breath  on  exertion,  and  for  some  months  before  her  death 
from  severe  attacks  of  pain  striking  from  the  front  of  the  left  chest  down 
the  inside  of  the  left  arm  to  the  Httle  finger,  with  great  tenderness  of  skin 
over  the  area  of  pain  after  the  attack  had  subsided.    She  had  erysipelas  in  the 


NODAL  BRADYCARDIA 


347 


face  in  1883  and  1885,  and  since  then  she  has  been  short  of  breath,  and 
with  a  tendency  to  sweUing  in  the  legs.  The  pulse  was  small,  quick,  and 
usually  regular,  but  I  occasionally  detected  an  extra-systole,  which  Fig.  246 
shows  to  be  auricular  in  origin.     There  was  a  large  pulsating  sweUing  on 


Fig.  241.     Simultaneous  tracings  of  jugular  and  carotid  pulses.     (Case  22.  1892.) 


Fig.  245.     Simultaneous  tracings  of  jugular  and  liver  pulses  ;   a,  auricular  wave  ; 
V,  ventricular  wave;    .r,  auricular  depression.     (Case  22.) 


Fig.  246. 


Simultaneous  tracings  of  tlie  jugular  and  radial  pulses,  showing  a  large  wave  (a') 
due  to  an  extra-systole  of  the  auricle.     (Case  22.) 


either  side  of  the  neck  near  the  sternal  end  of  the  clavicle,  Figs.  240  and 
241,  but  no  distinct  pulsation  in  the  veins  above  these  swellings.  When 
compared  with  the  carotid  pulse  there  were  seen  to  be  two  distinct  move- 
ments, the  one  larger  than  the  other,  to  each  carotid  pulse,  and  the  larger 
movement  could  be  observed  to  precede  that  of  the  carotid  pulse  (Fig.  241). 


348  DISEASES  OF  THE  HEART 

The  liver  could  be  felt  pulsating  just  below  the  ribs,  and  the  liver  pulse 
was  of  the  same  character  as  the  jugular  (Fig.  245). 

The  area  of  cardiac  dullness  was  increased,  extending  transversely  one 
and  a  half  inches  to  the  right  beyond  the  middle  line.  There  was  always 
present  a  long  murmur,  presystolic  in  time,  heard  best  at  the  apex ;  another, 
shorter  and  rougher,  of  a  different  character,  but  corresponding  in  time, 
was  heard  best  over  the  middle  of  the  sternum.  The  latter  murmur  was 
occasionally  absent  at  first,  but  ultimately  became  a  constant  pheno- 
menon. There  was  also  a  murmur,  systolic  in  time,  heard  at  the  apex. 
At  the  base  the  second  sound  was  reduplicated.  No  murmur  was  heard 
in  the  carotids,  but  there  was  a  distinct  sound  heard  over  the  pulsating 
swelling  in  the  neck  synchronous  with  the  pulsation  and  preceding  the 


Fig.  247.  Simultaneous  tracings  of  a  slight  movement  in  the  neck  and  of  the  radial  pulse. 
The  rhythm  is  now  continuously  irregular,  with  a  tendency  to  long  pauses.  The  tracing 
from  the  neck  was  taken  from  the  same  situation  which  gave  the  jugular  pulse  in  the  four 
preceding  figures,  and  demonstrates  the  absence  of  any  wave  due  to  the  auricle.  (Case  22. 
1895.) 

first  sound  of  the  heart.  This  sound  could  also  be  heard  under  the  clavicle 
and  over  Poupart's  ligament — i.e.  over  the  valves  of  the  subclavian  and 
femoral  veins.  The  jugular  and  subclavian  valves  being  competent,  the 
jugular  bulb  became  distended  into  a  ball-like  protrusion  over  the  inner 
end  of  the  clavicles,  and  the  pulsation  was  conspicuous  at  the  distance  of 
ten  yards. 

These  symptoms  persisted,  though  the  patient  became  gradually  weaker 
and  had  severe  attacks  of  angina  pectoris  on  the  shghtest  exertion.  (Figs.  1 1 
and  12  are  drawn  from  her.)  At  3  a.m.,  October  9,  1895,  she  awoke  and 
was  conscious  that  the  beating  in  her  neck  had  ceased.  She  called  my 
attention  to  this  next  morning,  and  on  examination  I  found  that  there 
was  now  no  pulsation  in  the  jugular  bulb.  Thus  Fig.  247  was  taken  from 
her  on  October  9,  1895,  and  the  receiver  was  held  over  the  place  where  the 
jugular  tracings  Figs.  240  and  241  were  obtained,  and  it  will  be  observed 
that  there  is  a  complete  absence  of  the  auricular  wave  which  is  so  marked 
in  these  tracings.  In  Fig.  247  there  is  only  a  faint  movement  due  to  the 
carotid,  and  possibly  at  the  beginning  of  this  tracing  a  sUght  ventricular 
venous  pulse  can  be  detected.     Careful  examination  showed  that  the  liver 


NODAL  BRADYCARDIA  349 

pulse  had  entirely  disappeared,  as  well  as  the  mitral  and  tricuspid  presystohc 
murmurs. 

On  October  13,  1895,  on  getting  out  of  bed,  she  fell  and  died. 

Before  removing  the  heart  at  the  post-mortem  examination  I  injected 
water  forcibly  into  the  superior  vena  cava,  and  the  water  could  not  pass 
beyond  the  jugular  valves,  but  distended  greatly  the  jugular  bulb.  The 
report  on  post-mortem  examination  of  the  heart  is  as  follows  : — Marked 
tricuspid  and  mitral  stenosis.  There  is  dilatation  of  the  apex  of  the  left 
ventricle,  pre-mortem  clot  in  apex  of  right  auricle.  The  series  of  sections 
of  a.-v.  biuidle  is  good,  and  shows  that  in  this  heart  the  node  at  the  com- 
mencement of  the  main  bundle  and  the  septal  divisions  were  uncommonly 
well  developed.  Main  bundle  healthy.  There  are  signs  of  great  venous 
back-pressure  in  the  capillaries  and  veins.  The  arteries  in  the  neighbour- 
hood of  the  bundle  are  not  thickened. 

I  have  dealt  with  this  subject  of  nodal  bradycardia  more  fully  else- 
where ^^^. 


APPENDIX  V 

Irregularities  in  Cardio-Sclerosis 

The  cause  of  the  variations  in  the  size  of  the  pulse-wave  is  a  subject  that 
needs  elucidation.  There  are  different  ways  in  which  it  may  arise.  The 
amount  of  blood  in  the  heart  at  the  time  of  the  systole  has  little  bearing  in 
the  cases  to  which  I  refer,  inasmuch  as  there  is  usually  plenty,  the  heart 
being  somewhat  dilated.  Apart  from  this,  the  difference  in  the  size  of  the 
pulse-wave  depends  on  the  strength  of  the  ventricular  contraction,  which  is 
determined  by  the  contractile  force  of  the  heart  muscle  and  the  number  of 
the  fibres  participating  in  the  contraction.  In  a  case  of  sinus  irregularity, 
especially  one  of  those  occurring  in  young  subjects,  we  find  that,  no  matter 
how  long  or  short  the  rest  preceding  the  contraction,  the  beats  themselves 
are  of  great  miiformity  (Figs.  73,  74,  79).  On  the  other  hand,  in  the  irregu- 
larities of  the  nodal  rhythm  we  find  the  size  of  the  beat  varies  with  the  length 
of  the  preceding  pause — the  longer  the  rest,  the  bigger  the  beat.  This 
implies  that  the  recovery  of  contractile  force  is  not  so  rapid  as  in  the  young 
with  a  sinus  irregularity.  This  is  the  explanation  adopted  in  §  179  to 
explain  the  pulsus  alternans.  But  this  explanation  is  not  the  only  possible 
one.  Muskens  maintains  that  the  smaller  size  of  the  beat  is  due  to  the 
fact  that  aU  the  fibres  do  not  contract,  that  there  is  a  block  preventing  the 
stimulus  for  contraction  from  reaching  all  the  fibres.  He  states  that  he 
has  been  able  to  produce  the  block  experimentally  in  the  frog's  heart.  On 
consideration,  I  have,  however,  adopted  the  view  of  Hoffmann  and  Wencke- 
bach in  regard  to  the  pulsus  alternans,  though  Muskens'  views  are  appHcable 
to  other  conditions  of  irregularity,  and  I  have  arrived  independently  at 
a  similar  conclusion.  I  refer  to  those  instances  in  which  there  are  varying 
sizes  in  the  pulse-wave,  and  in  which  big  waves  may  occur  after  a  short 
period  of  rest,  while  very  small  waves  may  occur  with  a  period  of  rest  of  the 
same  duration.  Here  the  smaller  beats  may  be  caused  by  some  fibres  of 
the  ventricle  faihng  to  contract  along  with  the  general  mass,  or,  as  recent 
electro-cardiograms  seem  to  show,  the  variation  in  the  size  of  the  beats  may 
be  due  to  the  starting  of  the  ventricular  contractions  from  different  places. 

I  have  not  been  able  to  work  out  the  matter  to  a  satisfactory  conclusion, 
but  I  have  used  it  as  a  means  of  forming  a  prognosis,  and  I  am  inclined  to 


IRREGULARITIES  IN  CARDIO-SCLEROSIS  351 

think  this  point  will  be  of  some  value.  The  matter  needs  further  considera- 
tion, and  the  different  factors  will  be  better  appreciated  by  the  study  of 
typical  irregularities,  whose  nature  can  be  analysed  with  a  greater  degree  of 
certainty.  A  good  deal  of  preliminary  work  will  have  to  be  done  to  under- 
stand the  different  causes  of  variations  in  the  strength  of  the  beats.  To  that 
end,  I  quote  here  two  cases  that  showed  during  life  a  somewhat  bewildering 
variety  of  irregularities,  and  I  demonstrate  how  these  can  be  referred 
to  their  various  causes  with  certainty.  The  citation  of  these  cases  also 
brings  out  certain  important  features  due  to  cardio-sclerosis  which  must  not 
be  looked  upon  as  exceptional,  for  I  have  seen  a  great  many  cases  exhibiting 
the  same  features  and  due  to  the  same  causes.  Briefly,  these  features  are 
variations  in  the  strength  of  the  contraction,  the  size  of  the  beat  depending 
on  the  period  of  rest  and  the  occurrence  of  extra-systoles. 

Case  23. — Male,  aged  fifty-seven.  Consulted  me  on  May  1,  1905,  com- 
plaining of  weakness  on  exertion,  a  sense  of  great  exhaustion  and  trembHng 
of  the  legs.  He  first  noticed  the  breathlfessness  three  years  ago  on  hurrying 
up  a  hiU,  when  he  had  a  severe  attack.  He  felt  fairly  well  until  six  months 
after,  since  which  time  the  breathlessness  is  very  easily  provoked. 

He  is  a  life-long  abstainer,  and  has  led  a  steady,  regular  life.  In  his 
younger  days  his  work  entailed  severe  bodily  effort,  but  for  the  last  twenty 
years  his  occupation  as  mill  manager  has  not  demanded  much  exertion. 
Twenty  years  ago  he  had  an  attack  of  '  inflammation  of  the  kidneys  '.  He 
is  a  powerfully  built  man  ;  face  greyish  in  colour,  pulse  rapid  (86  per  minute) 
and  hard,  the  artery  large  and  leathery  in  consistence.  Heart  is  enlarged, 
dull  to  the  nipple  line.  The  sounds  are  clear  and  distinct  ;  the  urine  con- 
tains a  large  quantity  of  albumen.  Blood-pressm-e,  210  mm.  Hg.  He  was 
directed  to  take  his  food  in  small  quantities,  and  to  chew  it  thoroughly  ;  to 
have  his  bowels  freely  opened  ;  and  he  was  put  upon  iodide  of  potassium. 
He  improved  wonderfully  for  a  time,  aU  the  albumen  disappearing  from  the 
urine,  but  he  began  to  relapse.  Abstinence  from  meat  was  tried  and  seemed 
to  do  him  good  for  a  short  time,  but  he  relapsed.  The  blood-pressure  records 
were  very  confusing,  sometimes  falling  to  145  and  rising  to  210,  and  this 
independent  of  drug  or  diet.  There  was  no  corresponding  improvement  in 
his  condition  with  the  fall  of  blood-pressure.  When  it  was  low  he  felt 
depressed,  and  sometimes  felt  very  well  when  it  was  high.  His  pulse 
was  usually  alternating  in  rhythm,  and  the  pecuharity  was  more  marked 
when  the  pressure  was  high.  When  the  irregularity  had  disappeared  with 
lowered  blood-pressure,  it  could  easUy  be  brought  back  by  running  up  a  flight 
of  stairs.  The  difference  in  pressure  between  the  beats  was  about  20  mm.  Hg. 
— that  is  to  say,  if  the  radial  pulse  was  obliterated  by  raising  the  pressure 


352 


DISEASES  OF  THE  HEART 


in  the  cuff  to  200  mm.  Hg.,  and  the  air  allowed  to  escape  from  the  cuff,  the 
large  beats  would  be  felt  coming  through  at  190  mm.  Hg.,  while  the  smaller 
would  not  be  felt  till  the  pressure  in  the  cuff  had  fallen  to  170  mm.  Hg.  (see 
Fig.  248). 


Fig.  248.  Tracing  taken  from  the  radial  artery  after  tlie  air  bag  connected  with  the  mano- 
meter had  obUterated  the  pulse  at  a  pressure  of  190  mm.  Hg.  The  air  was  allowed  to  escape 
gradually,  and  when  the  pressure  fell  to  180  mm.  Hg.  the  sphygmograph  received  the  stronger 
beats,  and  the  smaller  beats  came  tlu-ough  when  the  pressure  fell  to  170  mm.  Hg.  When  the 
pressure  in  the  air-bag  was  exhausted  the  pulse  tracing  showed  rhythmical  variation  in  the 
size  of  the  waves — that  is,  the  pulsus  alternans. 

Notwithstanding  the  alternating  rhythm,  the  pulse  rate  was  practically 
regular  (Figs.  249,  250,  also  Figs.  168-170).  In  May,  1906,  extra-systoles 
began  to  appear,  and  they  gave  a  peculiar  character  to  the  tracing.  Thus,  in 
Fig.  249  the  tracing  shows  a  perfectly  regular  rate  with  a  smaU  and  large 


RctdiaL 


JAiiiAMtWIMiiiAlIiABlll 


Fig.  249.  Typical  pulsus  alternans  with  ventricular  extra-systole  r'.  In  the  diagram 
it  is  shown  to  occur  prematurely  (downstroke  x  )  and  independently  of  the  auricular  stimulus. 
After  the  extra-systole  there  is  a  longer  pause,  and  the  alternating  character  of  the  pulse 
becomes  more  marked.     (Case  23.) 

beat  alternating,  except  in  the  centre,  where  there  are  two  small  beats  in 
succession.  On  measuring  the  tracing  it  wiU  be  found  that  the  second  of 
the  two  smaller  beats  (r')  occurs  a  little  too  early.  The  jugular  tracing  shows 
that  the  auricular  wave  (a)  is  perfectly  regular,  therefore  r'  is  a  ventricular 
extra-systole  and  after  it  there  is  a  longer  pause  than  normal,  so  that  the 
beat  after  the  pause  is  large,  and  the  succeeding  beat  smaller  than  the  other 


IRREGULARITIES  IN  CARDIO-SCLEROSIS  353 

beats  for  the  reason  explained  in  §  179.  This  increase  of  the  alternating 
character  of  the  rhythm  is  seen  in  Fig.  250.  Here  there  are  two  extra- 
systoles,  one  as  in  Fig.  249  after  the  small  beat,  and  the  other  after  a  large 
beat,  and  here  also  the  character  of  the  alternating  rhythm  is  more  marked 
after  the  extra-systole. 

The  patient  also  began  to  have  attacks  of  angina  pectoris,  which  I  have 
described  (Case  1,  Appendix  I).  He  became  restless  and  disturbed  at  night, 
and  the  attacks  of  pain  became  more  frequent,  until  he  was  put  upon  bromide 
of  ammonium,  when  he  began  to  sleep  better,  and  the  angina  disappeared. 
Towards  the  end  of  1906,  Che3nie-Stokes  respiration  appeared  (Fig.  6,  Plate  I), 
his  nights  became  very  restless,  and  he  could  only  be  reheved  by  opium  and 
chloral.  In  January  dropsy  set  in,  the  heart  dilated,  and  his  blood-pressure 
fell  permanently  to   150  mm.  Hg.  and  under.     The  virine  became  scanty. 


Fig.  250.     Here  there  are  two  extra-systoles  (r'  r'),  one  after  the  small  beat  and  the-other 
after  the  large  beat  of  the  alternating  rhythm.     (Case  23.) 

Various  preparations  of  digitalis  and  other  drugs  were  tried  with  little  good 
results,  and  the  patient  died  in  March,  1907.  Permission  was  only  given  to 
examine  the  heart,  and  the  following  is  the  report  of  the  post-mortem 
appearance  : — 

Musculature  of  ventricles. — Hypertrophied,  but  the  apical  half  of  ventricle 
is  fibrosed  and  dilated  ;  large  pre-mortem  clot  adherent  to  the  anterior  wall 
of  the  left  ventricle.  Thickness  of  wall  at  base,  18-22  mm.  ;  over  the  fibrosed 
area,  6-8  mm.  The  musculature  at  the  mouth  of  the  superior  vena  cava  is 
hypertrophied.  Taenia  terminahs  is  hj^ertrophied,  and  under  the  microscope 
shows  many  fibres  atrophied  and  fibrosed. 

Valves  and  orifices. — Mitral  cusps  thickened  ;  tricuspid,  pulmonary,  and 
aortic  healthy.  Auriculo-ventricular  orifices  smaller  than  normal,  due  to 
tonus  or  contraction  of  the  musculature  of  the  base. 

Arteries. — Patches  of  atheroma  in  aorta,  especially  at  orifices  of  coronary 
arteries.      Intense  endarteritis  of    left  coronary  artery,  diameter  6  mm., 

MACKENEIE  r  ^  g^ 


354  DISEASES  OF  THE  HEART 

lumen  2-5  mm.  ;  the  interior  is  especially  thickened.  The  right  coronary 
artery  is  not  so  much  affected.  All  the  arteries  of  the  heart  above  1-5  mm. 
in  diameter  are  affected  if  they  lie  outside  the  musculature  of  the  heart  ;  if 
surrounded  and  supported  by  the  musculature,  less  affected.  The  anterior 
inter-ventricular  artery  was  most  affected,  while  the  artery  to  the  a.-v.  bundle 
from  the  right  coronary  was  more  like  a  needle-prick. 

Remains  of  'primitive  cardiac  tissue. — Sino-auricular  node,  less  muscu- 
lature (more  fibrosed)  than  in  health,  still  not  marked.  The  a.-v.  bundle  is 
normal  in  size,  and  its  fibres  and  ceUs  are  normal. 

Case  24. — Male,  aged  seventy-two.  I  have  known  the  patient  for  over 
twenty-five  years  as  a  steady,  sober,  and  industrious  man.  He  worked  at  his 
occupation  as  an  engineer  up  to  within  a  year  of  his  death — though  in  later 
years  he  did  not  do  much  laborious  work.  He  had  a  slight  attack  of  hemi- 
plegia in  December,  1906.  He  consulted  me  in  June,  1907,  because  he  passed 
blood  in  his  urine.  Except  for  being  rather  short  of  breath,  he  felt  fairly  well. 
He  looked  a  hale  old  man.  His  radial  arteries  were  large  and  tortuous,  pulse 
full,  seemingly  regular.  His  heart's  dullness  extended  to  the  nipple  Une. 
The  sounds  of  the  heart  were  clear  except  for  a  musical  murmur,  systolic  in 
time,  heard  over  the  whole  heart  region,  but  loudest  in  the  aortic  area.  It 
varied  distinctly  in  loudness,  a  loud  murmur  alternating  with  one  less  loud. 
When  I  took  a  radial  tracing  it  showed  a  well-marked  pulsus  alternans.  He 
visited  me  several  times.  The  urine  became  quite  clear,  but  the  heart's 
condition  continued,  and  extra-systoles  were  sometimes  very  frequent, 
and  gave  to  the  pulse  the  appearance  of  extreme  irregularity  (Figs.  243, 
Plate  III,  244,  Plate  IV). 

Early  in  August  he  complained  greatly  of  attacks  of  bad  breathing  in  the 
night.  He  would  go  to  sleep  quite  quietly  and  then  awake  suddenly  with 
a  sense  of  suffocation,  and  sit  up  in  bed  breathing  heavily.  After  half  an 
hour  he  would  feel  easier,  but  could  not  lie  down,  and  had  to  be  propped  up 
in  bed.  These  attacks  occurred  on  several  occasions,  until  they  disappeared 
in  September,  when  his  legs  began  to  swell,  and  he  expectorated  quantities  of 
blood-stained  mucus  and  small  clots  of  blood.  His  heart's  dullness  extended 
two  inches  beyond  the  nipple  fine  ;  the  veins  of  the  arm  became  full.  Vene- 
section was  tried,  but  with  little  good  result,  and  he  died  in  October. 

An  analysis  of  the  tracings  taken  shows  that  the  irregularity  which  looked 
80  hopelessly  confused  was  due  to  the  mixture  of  the  pulsus  alternans  with 
extra-systoles.  Thus,  Fig.  242,  Plate  III,  shows  exactly  the  features  described 
in  Fig,  250,  where  there  are  several  extra-systoles  {r')  after  the  large  beat 
and  one  after  the  small,  with  an  increase  in  the  alternating  character  of 
the  rhythm  after  the  extra-systole.     Sometimes  the  extra-systole  appears 


IRREGULARITIES  IN  CARDIO-SCLEROSIS  355 

regularly  after  each  smaU  beat,  and  the  pulse  has  the  appearance  of  what 
used  to  be  called  a  trigeminal  pulse,  but  this  is  simply  due  to  a  big  beat  after 
the  long  pause  followed  by  a  small  normal  beat,  which  is  in  turn  followed  by 
a  ventricular  extra-systole  (Figs.  243,  Plate  III,  244,  Plate  IV).  The  jugular 
tracing  is  due  to  the  auricle  and  varies  at  times  in  rhythm,  so  as  to  give  rise 
to  the  suspicion  of  auricular  extra-systoles  at  ax.  The  patient  being  unable  to 
hold  his  breath,  the  jugular  pulse  varies  in  size  with  the  respiratory  move- 
ments. These  movements  are  recorded  in  Fig.  244,  Plate  IV.  The  respiratory 
movements  render  it  somewhat  difficult  to  be  sure  of  the  beginning  of  the 
auricular  systole,  and  I  have  endeavoured  in  the  intercalated  diagrams  to 
show  the  relative  time  of  the  auricular  and  ventricular  systoles,  and  the  time 
the  stimulus  took  to  pass  from  auricle  to  ventricle.  Except  in  Fig.  243,  the 
slanting  line  in  the  middle  space  represents  the  a-c  interval ;  in  Fig.  243  it 
represents  the  interval  between  the  auricular  systole  and  radial  pulse.  It 
will  be  seen  that  the  duration  of  the  interval  varies,  suggesting  that  the 
cardio-sclerosis  from  which  the  patient  suffered  also  affected  the  a. -v. 
bundle — a  suggestion  which  receives  some  support  from  the  post-mortem 
examination. 

Report  of  the  post-mortem  examination  of  the  heart  : — 
The  mitral  and  tricuspid  valves  show  no  pathological  changes.  The 
auricles  are  not  markedly  dilated  ;  the  coronary  sinus  is  filled  with  post- 
mortem clot.  The  ventricles  are  not  dilated,  except  at  the  apical  part 
of  the  left.  Both  coronary  arteries  show  a  thickening  of  their  coats,  with 
dilatation,  the  left  more  than  the  right,  and  the  anterior  interventricular 
branch  of  the  left  most  affected.  At  the  apex  of  the  left  ventricle  is  an  area 
showing  intense  fibrosis  with  deposits  of  premature  clot,  but  microscopic 
sections  show  the  Purkinje  and  inner  muscle-layer  healthy. 

The  a.-v.  node  and  bundle  show  a  fibrosis,  not  intense,  and  also  a  stretching 
of  the  bundle,  as  if  the  pars  membranacea  had  been  stretched.  There  is  no 
sign  of  cellular  change  in  the  bundle  or  node,  except  the  predominance  of 
the  fibrous  tissue  over  the  muscle  tissue — the  muscle-fibres,  instead  of  reticu- 
lating, being  stretched  and  parallel. 


Aa  2 


APPENDIX  VI 

The  Effects  of  Digitalis  on  the  Human  Heart 

In  Chapter  XXXIV  I  dealt  with  this  subject,  and  here  I  cite  a  few 
cases  to  illustrate  further  the  importance  of  this  line  of  investigation,  and 
to  call  attention  to  the  varying  ejBfects  of  digitalis  on  different  heart-lesions. 
I  wish  also  to  impress  upon  hospital  physicians,  by  these  illustrative  cases, 
the  great  opportunities  they  have  of  demonstrating  by  such  observations 
the  efifects  of  remedies.  The  experiences  I  detail  here  were  obtained  in  the 
course  of  my  daily  work  as  a  general  practitioner,  and  from  among  my 
private  patients.  The  difficulties  of  sufficiently  precise  observation  were 
insuperable,  so  that  of  necessity  my  work  lacks  the  precision  of  a  physio- 
logical experiment — a  precision,  however,  that  could  easily  be  attained 
were  the  patients  under  continual  observation  in  a  hospital  ward. 

This  Une  of  investigation  has,  I  am  glad  to  say,  been  adopted  by  several 
physicians,  and  John  Hay  ^^,  A.  G.  Gibson  ^^,  Hewlett  i°^,  Gossage^^,  Lewis  i^^, 
and  Guilleaume  ^^  have  demonstrated  equally  striking  results  from  the 
administration  of  digitaUs. 

In  the  interpretation  of  the  phenomena  given  here,  I  have  been  greatly 
assisted  by  Professor  Gushny,  whose  knowledge  of  the  physiological  action 
of  digitaUs  is  unrivalled. 

The  following  case  is  important,  as  it  shows  the  rhythm  of  the  heart 
changing  from  the  normal  to  the  nodal  rhyi:hm,  and  back  again  to  the 
normal,  and  the  difference  in  the  behaviour  of  the  heart  to  digitalis  under 
the  two  rhythms. 

Case  25. — Female,  aged  sixteen.  Seen  first  on  March  21,  1903.  Has  had 
rheumatic  fever,  and  for  some  years  has  suffered  from  breathlessness  and 
palpitation  on  exertion.  This  has  increased  lately,  and  there  is  shght 
oedema  of  the  legs.  There  is  marked  pulsation  of  the  veins  of  the  neck 
of  the  auricular  type  (Fig.  251).  The  pulse  is  small,  regular,  86  per  minute. 
There  is  great  heaving  of  the  left  chest  with  the  movements  of  the  greatly 
enlarged  heart.  The  apex  beat  is  large  and  diffuse,  and  felt  in  the  sixth 
interspace  and  in  the  anterior  axillary  line.  There  is  a  loud,  rough  systolic 
murmur  heard  over  the  whole  heart  and  round  to  the  back,  but  loudest 
at  the  apex.      With  rest  and  digitalis  she  rapidly  improved.      She  broke 


THE  EFFECTS  OF  DIGITALIS  ON  THE  HUMAN  HEART      357 

down  again,  and  a  note  on  January  9,  1904,  states  that  the  abdomen  is 
greatly  swollen,  the  liver  enlarged,  the  legs  oedematous,  and  the  urine 
scant.  The  radial  pulse  is  small,  soft,  and  rapid,  126  per  minute,  while 
the  Jugular  pulse  is  of  the  ventricular  type.  Under  digitalin  granules  she 
again  improved,  but  in  February  the  granules  were  stopped,  and  she  speedily 


Fig.  251.  This  and  the  following  seven  tracings  are  from  the  same 
patient.  Here  tlie  pulse  is  regular,  and  the  jugular  pulse  is  of  the  auricular 
type.     (Case  25,  March.  190.3.) 


Fig.  252.     The  jugular  pulse  is  now  of  the  ventricular  type.     (Case  25,   March  10,  1904.) 


Fig.  253.     The  jugular  pulse  is  still  of  the  ventricular  type,  but  under  the  action  of  digitalis 
the  radial  has  become  slow  and  irregular.     (Case  25,  March  18,  1904.) 

broke  down  again.  On  March  10,  1904,  the  condition  was  similar  to  that 
described  on  January  9,  the  radial  and  jugular  pulse-tracings  being  shown 
in_Fig.  251. 

She  was  prescribed  digitalin  granules,  one  per  day.  They  speedily 
took  effect,  and  on  March  18  the  pulse  had  become  slow  and  irregular 
(Fig.  253).     The  urine  had  greatly  increased  in  quantity,  the  abdomen  and 


358 


DISEASES  OF  THE  HEART 


liver  had  diminished  in  size,  and  all  signs  of  dropsy  had  gone.  The  digitalis 
was  continued  till  March  28,  one  granule  being  taken  every  second  day, 
and  she  continued  in  fair  health,  the  pulse  still  slow  and  irregular,  as  shown 
by  Fig.  254,  which  was  taken  on  March  26. 

The  digitahn  was  stopped  on  March  28.      Four  days  after  stopping  it 
the  pulse  had  increased  to  85  per  minute,  though  she  felt  stiU  fairly  weU. 


Fig.  254.  Shows  the  characteristic  effect  of  digitalis  being  maintained.  (March  26,  1904.) 
The  jugular  tracing  shows  the  nature  of  the  arrhythmia,  and  the  coupled  beats  resemble  the 
tracings  in  Figs.  153,  157,  159,  and  160.     (Case  25.) 

On  April  5 — that  is,  eight  days  after  stopping  the  digitalin — the  rate  of 
the  heart  had  increased  to  120  beats  per  minute,  the  pulse  had  become 
small  and  weak,  and  the  jugular  distension  had  increased  (Fig.  255),  The 
other  signs  of  heart  failure  were  beginning  to  show  themselves.  She  was 
again  put  on  digitalin,  one  granule  per  day.     On  April  9  the  pulse  was  still 


Fig.  255.  Eight  days  after  stopping  the  digitalin,  failure  of  compensation  again  set  in, 
the  pulse  here  being  120  per  minute,  and  the  jugular  pulse  being  still  of  the  ventricular  type. 
(Case  25,  April  5,  1904.) 

120  per  minute.     On  April  11  it  was  130,  on  April  14  it  had  again  become 
slow  and  irregular  (Fig.  256). 

The  digitaUn  was  again  stopped,  but  as  the  pulse  began  to  increase  in 
rate,  on  April  17,  one  granule  per  day  was  prescribed.  The  patient  con- 
tinued in  fair  health,  but  as  the  pulse  did  not  slow  down  satisfactorily,  on 
May  1  I  doubled  the  dose.  I  did  not  take  any  further  tracings  tiU  May  14, 
contenting  myself  with  watching  for  the  slowing  of  the  pulse.  Finding  it 
did  not  yield  as  before  to  the  increased  doses  of  digitahn,  I  took  tracings 


THE  EFFECTS  OF  DIGITALIS  ON  THE  HUMAN  HEART      359 

on  this  day,  and  found  a  perfectly  regular  radial  pulse,  while  the  jugular 
pulse  had  completely  changed  its  character,  being  now  of  the  auricular 


Fig.  256.     Nine  days  after  beginning  the  digitalis  the  characteristic  effect  is 
reproduced.     (Case  25,  April  14,  1904.) 


Fig.  257.  With  continued  use  of  digitalis  the  auricles  resume  the  inception  of 
the  rhythm  of  the  heart,  as  shown  by  the  fact  that  here  the  jugular  pulse  is  of  the 
auricular  type.     (Case  25,  May  15,  1904.) 


Fig.  260.  Shows  a  jugular  pulse  of  the  auricular  type  with  the 
occasional  occurrence  of  a  ventricular  extra-systole.  The  auricular 
waves  {a  and  a')  occur  at  regular  intervals,  while  the  small  waves  ( x ) 
in  the  radial  occur  prematurely.  The  larger  size  of  a'  is  due  to  the  fact 
that  when  the  auricle  contracts  the  ventricle  is  already  in  systole,  and 
therefore  cannot  receive  the  auricular  contents,  which  are  thus  sent  back 
into  the  veins,  producing  tills  larger  wave.     (Case  25,  January  2,  1905.) 

type that  is,  the  auricle  had  again  resumed  its  normal  action  and  the 

heart  chambers  contracted  in  their  normal  sequence.     Occasionally,  for 
a  short  period,  it  would  show  a  shght  alternating  rhythm,  as  in  Fig.  257. 


360  DISEASES  OF  THE  HEART 

The  digitalin  was  stopped,  and  the  patient  continued  in  fair  health  for 
some  ^months.  The  jugular  pulse  continued  of  the  auricular  type,  and  the 
pulse  was  quite  regular  until  her  death  in  December,  1905,  except  during 
a  short  period  shortly  to  be  described.  On  December  18,  1904,  she  was 
again  beginning  to  get  oedema  of  the  legs,  and  the  abdomen  began  to  swell, 
and  she  was  very  breathless.  The  pulse  was  small,  soft,  and  rapid,  110  per 
minute,  and  the  jugular  pulse  was  still  of  the  auricular  type.  She  was 
prescribed  one  granule  of  the  digitalis  per  day.  No  improvement  had  taken 
place  by  December  27,  when  she  was  ordered  to  take  two  granules  per  day. 
By  January  2,  1905,  the  rate  had  fallen  to  80,  as  a  rule  quite  regular,  but 
occasionally  an  extra-systole  of  ventricular  origin  would  occur  (Fig.  260), 
Sometimes  for  a  short  period  these  ventricular  extra-systoles  would  appear 
after  every  second  beat.  The  digitaHs  was  stopped,  and  the  arrhythmia 
disappeared. 


Fig.  262.    Simultaneous  tracings  of  the  jugular  and  radial  pulses.    The  jugular  pulse  is  of  the 
auricular  type  and  the  distension  of  the  veins  obscured  the  carotid.    (Case  26,  April  22,  1907.) 


Case  26. — Male,  aged  eleven,  seen  by  me  on  April  26,  1907  ;  complained 
of  weakness,  shortness  of  breath,  and  palpitation.  He  had  rheumatic  fever 
at  the  age  of  seven.  His  pulse  was  rapid  (110  per  minute),  small,  and  regular 
(Fig.  259).  The  heart  was  enlarged,  the  apex  beat  diffuse,  extending  one  inch 
beyond  the  nipple  line.  There  was  a  long,  loud  systolic  mitral  murmur. 
There  was  only  a  faint  pulse  in  the  distended  jugular,  and  I  had  some 
difficulty  in  getting  a  tracing  (Fig.  262).  It  was  of  the  auricular  form, 
and  the  a-c  interval  (space  A)  was  rather  greater  than  would  normally 
appear  with  so  rapid  a  heart-rate.  I  prescribed  digitalin  granules,  one 
granule  per  day,  and  after  taking  ten  granules  he  became  very  sick  and 
vomited,  and  his  pulse  became  slow  and  irregular.  The  granules  were 
at  once  stopped,  and  after  the  sickness  subsided  the  boy  felt  much  better 
and  remained  in  a  fair  state  of  health  up  to  the  last  time  I  saw  him,  in 
November,  1907.  I  took  a  large  number  of  observations  when  the  heart 
was  slow  from  the  effects  of  digitalis,  and  the  irregularities  were  all 
due  to  the  same  cause — the  di'opping  out  of  ventricular  systoles  as  shown 


THE  EFFECTS  OF  DIGITALIS  ON  THE  HUMAN  HEART      361 

in  Fig.  264.  I  have  constructed  a  diagram  showing  the  character  of  the 
irregularity,  and  it  can  be  seen  that  the  auricle  pursues  a  regular  course  ; 
that  the  a-c  interval  varies,  being  shorter  after  a  pause  and  lengthening 
until  a  beat  drops  out  (Fig.  269). 


Fig.  264.  The  auricular  wave,  a  and  a',  is  regular.  .The  long  pauses  in  the  radial  tracing 
are  due  to  dropping  out  of  the  ventricular  contractions — the  stimulus  from  the  auricle  being 
blocked  at  tlie  a-v  bundle  (see  diagram,  Fig.  269).  Note  the  variation  in  the  a-c  interval 
(spaces  .4).     (Case  26,   April  26,  1907.     After  10  digitalin  granules.) 

Fig.  269.  Diagram  showing  the  auricular  and  ventricular  systoles  from  Fig.  264.  Note 
the  lengthened  a-c  interval  before  and  the  shortened  a-c  interval  after  the  dropping  out  of 
the  ventricular  contraction.     (Case  26.) 


Fia.  270.     The  jugular  tracing  shows  a  wide  a-c  interval  (space  A ).    (Case  27.    Before  digitalis.) 

Case  27. — Male,  aged  twenty-five,  consulted  me  for  a  stiffness  and 
swelling  in  sundry  joints,  wrists,  ankle,  and  knee,  on  May  4,  1906.  The  heart 
was  rapid  in  its  action,  120  per  minute  ;  slightly  enlarged  with  systolic 
mitral  and  tricuspid  murmurs.  There  was  marked  pulsation  in  the  neck, 
of  which  Fig.  270  is  a  tracing.  The  movement  due  to  the  carotid  was 
always  large,  and  forms  a  marked  feature  (wave  c  in  aU  the  tracings).  In 
the  course  of  the  next  fortnight  there  gradually  developed  double  aortic 


362 


DISEASES  OF  THE  HEART 


murmurs.  By  May  23,  under  treatment,  he  had  gradually  improved,  the 
rate  of  the  heart  falling  to  90  beats  per  minute. 

As  the  a-c  interval,  space  A,  in  Fig.  270,  showed  a  delay  in  the  function 
of  conductivity,  I  reasoned  that  the  carditis  had  probably  affected  the 
a.-v.  fibres,  and  had  depressed  the  function  of  conductivity.  I  administered 
digitalin  granules,  one  to  be  taken  three  times  a  day. 

I  kept  him  under  observation,  but  could  detect  no  change  in  the  heart's 
action  until  May  30,  after  he  had  taken  nineteen  granules.  On  this  date 
I  found  the  pulse  at  times  very  irregular.  Fig.  271  is  a  tracing,  showing 
the  nature  of  the  irregularity.  Between  the  jugular  and  radial  pulses 
I  have  intercalated  a  diagram  illustrating  the  events  in  the  tracing  from 
the  neck.      It  will  be  noticed  that  before  a  ventricular  beat  drops  out 


maam^mmam 


Fig.  271.  After  taking  nineteen  digitalin  granules  the  pulse  became  irregular,  wliich  the 
intercalated  diagram  shows  to  be  due  to  dropping  out  of  the  ventricular  systoles — a  mild  form 
of  heart-block.     (Case  27.) 


there  is  a  gradual  lengthening  of  the  a-c  interval,  and  that  the  dropping 
out  of  the  ventricular  systole  is  manifestly  due  to  an  increased  depression 
of  the  conductivity  of  the  fibres  joining  a  and  v — that  is  to  say,  the 
stimulus  from  the  auricle  is  blocked  before  it  reaches  the  ventricle. 
I  stopped  the  digitalin,  and  a  few  days  later  all  signs  of  irregularity  had 
disappeared.  The  patient  himself  was  conscious  when  his  heart  was  irregu- 
lar, and  I  remarked  to  him  that  the  irregularity  had  gone  ;  he  repUed, 
*  I  can  bring  it  back.'  I  asked  him  how  he  could  do  so,  and  he  said,  '  By 
swallowing.'  I  asked  him  to  swallow,  and  he  did  so,  and  immediately 
I  detected  long  pauses  in  his  pulse,  while,  on  auscultation  of  the  heart, 
no  sounds  were  heard  during  the  pauses.  I  took  a  large  number  of  tracings 
for  an  hour  and  a  half,  during  which  time  he  swallowed  forty  or  fifty  times, 
and  the  alteration  in  the  pulse-rate  never  failed  to  appear.  The  character- 
istic changes  are  seen  in  Figs.  258,  Plate  IV,  and  259,  Plate  IV.  After 
swallowing  there  are  each  time  three  regular  beats,  then  the  pulse  slows 
in  the  manner  shown  in  the  tracings.     After  two  or  three  slow  beats  the 


THE  EFFECTS  OF  DIGITALIS  ON  THE  HTOIAN  HEART       363 

rate  of  the  heart  increased  for  six  or  seven  beats,  then  gradually  slowed  in 
the  manner  shown  in  the  latter  part  of  the  tracings.  Occasionally  during 
the  secondary  slowing  one  ventricular  systole  would  drop  out,  as  is  shown 
in  Fig.  259,  Plate  IV.  In  Fig.  259,  Plate  IV,  I  have  intercalated  a  diagram 
which  shows  the  nature  of  the  arrhythmia,  and  it  can  there  be  seen  that 
the  long  pauses  in  these  tracings  are  preceded  by  an  increase  of  the  a-c 
interval,  just  as  happened  when  the  patient  was  under  the  influence  of 
digitalis  (Fig.  271),  and  that  the  dropping  of  the  ventricular  systole  was 
due  to  a  block  of  the  stimulus  from  auricle  to  ventricle.  The  numbers 
given  under  the  radial  tracings  in  Fig.  259,  Plate  IV,  represent  tenths  of 
seconds,  and  from  these  numbers  the  manner  in  which  the  rate  of  the  pulse 
varies  can  better  be  realized. 

The  susceptibihty  of  the  heart  to  the  act  of  swallowing  continued  for 
a  week,  then  entirely  disappeared.  There  is  no  doubt  it  arose  through 
reflex  stimulation  of  the  vagus  induced  by  the  act  of  swallowing.  The 
analogy  between  the  effects  of  digitahs  and  of  reflex  stimulation  of  the 
inhibition  by  swallowing  appears  worthy  of  note,  as  it  indicates  that  the 
action  of  the  drug  here  is  exerted  through  its  effects  on  the  inhibitory  centre, 
and  not  through  the  changes  it  induces  in  the  heart  muscle  directly.  Digi- 
talis, as  is  generally  known,  affects  the  vagus  centre  and  also  the  myocardium, 
and  it  is  often  difficult  to  determine  which  is  the  factor  in  its  therapeutic 
effects.  This  case,  taken  along  with  Case  28,  seems  to  give  valuable  data 
on  this  question. 

The  cases  I  have  quoted  here  and  in  Chapter  XXXIV  present  the  more 
common  effect  of  digitahs  on  diseased  hearts.  Other  cases  crop  up  that 
show  different  changes,  some  of  which  are  capable  of  being  analysed,  so 
that  one  can  teU  with  fair  certainty  what  is  happening,  though  the  manner 
in  which  the  phenomena  are  produced  remains  obscure.  These  cases  are 
nearly  all  due  to  rheumatic  affection  of  the  heart.  The  following  case 
showed  a  series  of  pecuUar  symptoms,  and  I  select  the  most  significant 
of  these.  It  is  impossible  here  to  give  fully  the  whole  of  the  observations 
in  this  case,  for  verbal  description  is  of  httle  use,  the  tracings  alone  demon- 
strating the  changes,  and  I  have  taken  as  many  observations  on  this  patient 
as  would  fill  a  goodly  volume.  I  am  also  unfortunately  unable  to  give 
minute  particulars  as  to  the  quantity  of  the  drug  that  produced  the  symp- 
toms, for  the  patient  was  not  confined  to  bed,  and,  hving  some  distance 
from  me,  visited  me  at  irregular  intervals.  Being  the  wife  of  a  working 
man  she  had  her  household  duties  to  perform,  and  when  feeling  better 
did  not  trouble  to  come  to  see  me.  As  the  improvement  in  her  condition 
always  coincided  with  the  changes  in  the  heart's  rhythm,  I  was  not  able 


364  DISEASES  OF  THE  HEART 

to  note  the  beginning  of  the  changes  and  the  quantity  of  the  drug  that 
induced  them. 

The  drugs  used  in  this  case  were  the  digitalis,  squill,  and  calomel  pills, 
digitaHn  granules,  and  the  tincture  of  strophanthus.  So  far  as  the  heart's 
irregularities  were  concerned,  each  form  of  medicine  produced  the  same 
result.  The  patient  preferred  the  digitaUs,  squill,  and  calomel  piU,  as  it 
was  the  speediest  in  diminishing  the  dropsy  by  inducing  an  increased  flow 
of  urine,  and  a  little  diarrhoea,  and  the  appearance  of  the  diarrhoea  was 
always  accompanied  by  improvement  in  the  breathing. 

When  not  taking  any  drug  the  heart  was  quite  regular  in  its  rhjrthm 
until  the  last  month  of  these  observations,  when  the  nodal  rhythm  became 
established.     Under    the   influence    of   the    digitalis    or    strophanthus    the 
.  following  irregularities  appeared  : — 

(1)  Nodal  rhjrthm  (transient). 

(2)  Slowing  of  the  auricles  and  ventricles,  the  whole  heart  participating 
in  the  slow  action. 

(3)  After  a  long  pause  the  heart's  contraction  started  feebly,  and 
increased  in  strength  with  each  succeeding  beat  (staircase  phenomenon). 

(4)  Extra-systoles. 

The  a-c  interval  when  the  heart  was  not  under  the  influence  of  the  drug 
was  always  greatly  increased,  and  the  digitalis  did  not  increase  the  delay, 
as  in  the  cases  already  quoted.  During  the  long  pauses  the  a~c  intervals 
became  greatly  shortened.  As  there  was  in  this  case  a  marked  presystolic 
murmur,  the  relationship  of  this  murmur  to  the  first  sound  varied  with 
the  length  of  the  a-c  interval,  sometimes  being  separated  from  the  first 
sound,  sometimes  running  up  into  it,  and  sometimes  not  being  distinguish- 
able from  it  (see  Fig.  265,  Plate  V).  During  the  nodal  rhythm  the 
presystolic  murmur  disappeared. 

Case  28. — Female,  aged  twenty-eight.  Consulted  me  April  24,  1907, 
complaining  of  swelling  of  the  abdomen,  shortness  of  breath,  and  palpitation. 
She  began  to  feel  ill  in  November  of  the  previous  year  ;  she  had  rheumatic 
fever  fifteen  years  previously.  The  face  is  dusky,  the  breathing  laboured, 
the  legs  and  abdomen  swollen.  She  passes  little  urine.  There  is  rapid  pulsa- 
tion in  the  veins  of  the  neck — two  to  each  radial  pulse  (Fig.  272) — the  pulse 
is  small  and  regular,  blood-pressure  100  mm.  Hg.  A  thrill  systohc  in  time  can 
be  felt  over  the  upper  part  of  the  chest.  The  movement  of  the  heart  farthest 
to  the  left  is  three  inches  beyond  the  nipple,  and  shows  an  indrawing  during 
ventricular  systole  (giving  rise  to  an  inverted  cardiogram).  The  heart's 
dullness  extends  half  an  inch  to  the  right  of  the  sternum.  At  the  apex 
there  is  heard  a  presystolic  murmur,  a  diastolic  murmur,  and  a  reduplicated 


THE  EFFECTS  OF  DIGITALIS  ON  THE  HUIVIAN  HEART     365 

second  sound.  At  the  base  there  is  a  loud,  rough  murmur  systolic  in  time, 
heard  also  over  the  carotid.  There  is  also  a  sHght  diastohc  murmur  at  the 
aortic  area.  Over  the  heart's  dullness  inside  the  nipple  there  is  another 
murmur  systohc  in  time,  and  while  hstening  one  could  imagine  that  two 
hearts  were  working,  a  series  of  sounds  being  heard  immediately  under  the 
stethoscope,  while  another  series  of  sounds  could  be  heard  faintly  and 
seemingly  at  a  distance. 

Sometimes  when  the  heart  was  regular  but  slow,  a  confusing  change 
took  place.  During  the  diastole  of  the  heart  there  was  a  sudden  increase 
in  the  intensity  of  the  diastoUc  murmur,  in  fact  a  mid-diastohc  murmur 
followed  after  a  pause  by  the  first  sound.     When  I  drew  the  position  of 


Fig.  272.  Shows  two  pulsations  in  the  jugular  tracing  (a  and  v)  to  one  radial  pulse.  The 
a-c  interval  (space  A)  is  increased.  The  shading  shows  the  sounds  of  the  heart  and  the 
murmiurs  present  at  the  apex,  viz.  a  presystoUc  murmur  separated  by  a  brief  interval  from 
the  first  sound,  a  reduplicated  second  sound  followed  by  a  diastohc  murmur.  These  features 
of  the  jugular  pulse  and  sounds  and  murmurs  were  always  present  when  the  patient  was 
not  under  the  influence  of  digitahs  until  the  final  establishment  of  the  nodal  rhythm  as  shown 
in  Fig.  268,  Plate  V.     (Case  28.) 

the  murmur  under  a  tracing  I  found  it  corresponded  to  the  position  of  the 
auricular  wave  in  the  jugular  tracing  (Fig.  272),  and  no  doubt  it  was  due 
to  the  auricular  systole.  When  the  heart  became  very  slow,  because  of 
the  digitalis,  the  longer  rest  gave  the  a. -v.  fibres  time  to  recover  and  the 
murmur  was  heard  nearer  and  nearer  the  first  sound,  and  sometimes  it 
ceased  to  be  heard.  This  only  happened  when  the  heart  became  very  slow 
and  the  auricular  wave  in  the  jugular  approached  quite  close  to  the  carotid. 
These  changes  in  the  sounds  and  position  of  the  auricular  wave  are  seen  in 
Fig.  265,  Plate  V.  I  am  aware  that  this  explanation  may  appear  fanciful, 
but  it  is  the  outcome  of  long  and  patient  study  on  the  part  of  myself  and 
some  of  my  colleagues.  My  colleague.  Dr.  Crump,  who  is  a  very  skilled 
auscultator,  verified,  after  a  long  examination,  these  changes  in  the  position 
of  this  auricular  systole,  and  when  shown  the  tracings  which  were  taken 


366  DISEASES  OF  THE  HEART 

while  he  was  Ustening,  agreed  to  the  place  of  the  murmur  indicated  by 
the  shading  in  Fig.  265,  Plate  V.  I  dwell  at  length  upon  this  on  account 
of  the  views  that  are  held  by  some  able  clinicians  that  the  presystoUc 
murmur  in  mitral  stenosis  is  not  due  to  the  auricular  systole. 

The  patient  was  put  on  the  digitaUs,  squill,  and  calomel  pill,  one  taken 
three  times  a  day.  On  May  1,  after  taking  eighteen  pills,  she  was  passing 
more  urine.  She  felt  much  better  on  the  8th — the  swelUng  had  gone  from 
the  abdomen  and  the  legs  were  less  in  size.  On  the  15th  the  swelling  had 
all  gone,  she  had  a  little  diarrhoea  and  felt  sickly,  but  breathed  easier  and 
was  able  to  walk  better.  The  heart  was  slow  and  irregular.  On  examina- 
tion there  was  only  one  wave  visible  in  the  jugular,  and  when  recorded 
it  was  found  synchronous  with  the  carotid  pulse  (Fig.  261,  Plate  IV). 
There  was  no  presystolic  murmur,  but  only  a  long  diastoUc  murmur  at  the 
apex,  diagrammaticaUy  represented  in  Fig.  261,  Plate  IV.  The  tracing 
shows  the  jugular  pulse  to  be  of  the  ventricular  type,  i.  e.  the  heart  has 
taken  on  the  nodal  rhythm.  The  pills  were  stopped,  but  the  heart  was 
still  irregular  on  the  19th.  On  the  26th  it  was  regular  and  the  jugular 
pulse  double  waved  as  in  Fig.  272.  She  felt  better,  but  the  legs  and  abdo- 
men were  swelhng  again.  Digitalin  granules  were  prescribed,  one  three 
times  a  day.  On  the  31st  the  pulse  became  irregular  and  tracings  taken 
on  this  day  and  on  June  2  showed  that  it  was  due  to  the  slowing  of  the 
whole  heart  (Figs.  273,  and  263  Plate  IV).  On  June  4  the  heart  had  again 
taken  on  the  nodal  rhythm  (Fig.  261,  Plate  IV),  which  persisted  until  the 
17th,  when  the  auricular  contractions  appeared  and  the  heart  showed 
frequent  pauses.  She  was  taking  one  granule  of  digitalin  per  day  until 
the  23rd,  when  it  was  stopped,  and  on  the  28th  the  heart  was  found  rapid 
and  regular  and  the  pulsation  in  the  veins  double  waved,  as  in  Fig.  272. 
Up  till  November  4  these  reactions  due  to  digitalis  continued  to  appear  ; 
sometimes  the  nodal  rhythm  would  appear  and  sometimes  the  long  pauses 
as  in  Figs.  273,  and  263  Plate  IV,  and  occasionally  extra-systoles  as  in 
Figs.  266  and  267,  Plate  V.  A  few  days  after  stopping  the  digitalis  the 
heart  invariably  became  regular.  On  November  6,  after  digitalis  treat- 
ment had  ceased,  the  heart  assumed  the  nodal  rhythm  (Fig.  268,  Plate  V) 
continuously,  beating  rapidly,  but  it  could  be  slowed  by  digitalis  or 
strophanthus. 

Interpretation  of  tracings. — The  tracings  showing  the  nodal  rhythm 
(Figs.  261,  Plate  IV,  and  268,  Plate  V)  call  for  no  special  description, 
as  they  resemble  the  tracings  of  the  ventricular  venous  pulse  so  fully 
described  elsewhere.  The  only  point  which  seems  novel  is  that  when  it 
began  under  the  influence  of  digitalis  (Fig.   261,  Plate  IV)  it  was  a  slow 


THE  EFFECTS  OF  DIGITALIS  ON  THE  HUMAN  HEART     367 

rhythm  resembling  in  some  respects  the  cases  of  nodal  bradycardia 
(Appendix  IV).  On  the  other  hand,  when  it  started  independently  of 
digitalis  the  heart's  action  was  rapid,  as  is  usually  the  case. 

In  Fig.  273  there  is  a  long  pause  in  which  the  whole  heart  stands  still  ; 
during  these  pauses  no  sound  could  be  heard  and  the  tracings  show  the 
auricles  arrested  as  weU  as  the  ventricle — differing  thus  from  heart-block. 
I  observed  that  after  the  long  pause  the  radial  beats  were  at  first  small, 
then  gradually  increased  in  size,  but  as  the  pulse  was  small  and  soft  the  ink 
polygraph  did  not  show  the  beats  well  ;  I  therefore  took  several  tracings 
with  the  Dudgeon  sphygmograph,  of  which  Fig.  263,  Plate  IV,  is  a  good 
instance.  Here  the  gradual  increase  of  the  radial  pulse  after  the  long  pause 
is  very  evident.  The  pauses  lasted  sometimes  from  three  to  four  seconds. 
Thus  in  Fig.  263,  Plate  IV,  one  pause  lasts  fifteen-fifths  of  a  second,  while 


Fig.  273.     Shows  the  temporary  arrest  of  the  whole  heart  from  digitalis.     (Case  28.) 

the  other  lasts  nineteen-fifths  of  a  second.  This  standstill  of  the  whole 
heart  is  probably  due  to  vagus  stimulation.  The  staircase  phenomenon 
after  the  pause  has  been  shown  experimentally  to  occur  after  a  vagus 
standstill  of  the  whole  heart,  and,  according  to  Gaskell,  arises  in  two  ways  : 

(1)  From  exhaustion  of  contractiUty — the  vagus  stimulation  depresses  aU 
the  functions  and  their  restoration  is  gradual,  that  of  restoration  of  con- 
tractihty  being  showTi  by  a  gradUal  increase  in  the  strength  of  the  beat. 

(2)  From  depression  of  conductivity,  the  stimulus  for  contraction  not 
spreading  throughout  the  whole  heart,  but  reaching  at  fii'st  a  limited 
number  of  fibres,  and  gradually  reaching  more  and  more  until  they  all 
respond. 

The  pauses  were  not  always  so  long  as  in  Fig.  263,  Plate  IV,  and  the 
heart  would  beat  slowly  for  a  short  period.  When  this  happened,  the  relation 
of  the  auricular  systole  to  the  ventricular  underwent  an  interesting  change. 
As  I  have  already  remarked,  the  a-c  interval  was  always  increased  in  this 
patient,  but  digitahs  did  not  interfere  with  the  conduction  of  the  stimulus 


368  DISEASES  OF  THE  HEART 

from  auricle  to  ventricle.  When  the  heart  acted  slowly  the  a.-v.  fibres 
obtained  a  long  rest,  with  the  result  that  the  a-c  interval  gradually  dimin- 
ished until  it  was  scarcely  perceptible.  Fig.  274  shows  the  carotid  and 
radial  pulses.  The  carotid  is  taken  from  luider  the  right  jaw,  but  the 
wave  (a)  due  to  the  auricular  systole  is  present  in  the  tracing.  When  the 
heart  was  beating  at  the  more  rapid  rate,  the  a-c  interval  (spaces  A)  was 
nearly  two-fifths  in  duration,  whereas  when  beating  at  the  slower  rate  it 
became  less  than  one-fifth  in  duration.  This  is  brought  out  particularly 
well  in  Fig.  265,  Plate  V,  where  the  auricular  wave,  a,  gradually  approaches 
the  carotid  and  ventricular  wave  tiU  it  is  not  discernible  as  a  distinct  wave. 
It  was  during  periods  such  as  this  that  Dr.  Crump  and  I  made  out  the 


Fig.  274.  The  upper  tracing  was  taken  high  up  in  the  neck  and  shows  a  slight  auricular 
wave  (a)  preceding  the  carotid  pulse  (c).  After  a  long  pause  the  a-c  interval  (space  A)  is 
much  diminished.     (Case  28.) 

change  in  the  relation  of  the  presystohc  murmur  to  the  first  sound  and 
its  apparent  cessation — as  shown  by  the  shading  underneath  the  jugular 
tracing. 

It  may  be  taken  as  certain  that  in  this  patient  the  marked  slowing  and 
long  pauses  were  inhibitory  in  origin.  But  the  inhibition  appeared  not  to 
involve  the  a.-v.  fibres,  for  their  conductivity  was  not  reduced,  this  proving 
that  the  drug  acts  on  the  a.-v.  fibres  through  its  action  on  the  inhibitory 
function  and  not  through  its  direct  effects  on  the  heart  muscle.  (Compare 
Case  27.) 

Another  phase  that  occasionally  occurred  during  the  irregular  period 
was  the  appearance  of  extra-systoles.  Figs.  266  and  267,  Plate  V  (Fig.  267 
is  a  continuation  of  Fig.  266),  are  characteristic  examples,  and  show  that 
the  extra-systoles  are  probably  of  ventricular  origin,  though  the  pauses 
following  the  extra-systoles  are  of  varying  duration,  due  to  the  influence 
of  the  digitaUs  on  the  sinus. 

This  case,  as  I  have  said,  is  an  exception  to  the  general  rule  that  when 
there  is  a  delayed  a-c  interval  digitalis  increases  it  and  produces  blocking 


THE  EFFECTS  OF  DIGITALIS  ON  THE  HUMAN  HEART     369 

of  the  systoles  between  auricle  and  ventricle.  I  have  carefuUy  considered 
whether  there  may  not  have  been  blocking  between  the  sinus  and  auricle, 
as  has  been  shown  to  occur  by  Wenckebach  ^-^  and  Hewlett  202.  i  can  find 
no  reason  for  suspecting  such  a  thing  here,  particularly  as  the  slow  periods 
have  no  such  regularity  as  to  lead  one  to  infer  that  the  sinus  was  beating 
at  regular  intervals.  In  this  case  the  whole  heart  seemed  affected  by  the 
digitahs,  but  on  exceptional  occasions  the  ventricles  escaped  and  produced 
extra-systoles. 

Records  of  blood-pressure  showed  generally  a  faU  (100  mm.  Hg.)  when 
there  was  much  dropsy,  and  a  rise  with  slowing  of  the  heart  to  135  or 
140  mm.  Hg.  Sometimes,  however,  the  pressure  was  130  with  dropsy, 
and  no  increase  occurred  with  its  disappearance  and  the  coincident 
improvement  of  the  patient's  condition  after  taking  digitalis. 


MACKENZIE  3  |) 


APPENDIX  VII 

The  Electro-cardiogram  * 
By  Thomas  Lewis,  M.D.,  M.R.C.P. 

1.  The  relation  of  contraction  to  electric  changes  in  muscular  tissue. 

For  many  years  it  has  been  known  that  muscular  activity  is  accompanied 
by  electric  changes.  When  a  strip  of  somatic  musculature  is  stimulated 
at  one  end,  and  contraction  is  induced  at  the  point  of  stimulation,  this  point 
becomes  electro-negative  to  the  resting  or  inactive  end.  If,  as  a  result  of 
the  excitation,  a  wave  of  contraction  is  propagated  in  the  muscle,  then,  as 
each  successive  segment  enters  upon  the  contractile  state,  each  segment 
becomes  relatively  electro-negative.  The  change  in  potential,  or  the  varia- 
tion in  the  current  produced  by  it,  may  be  registered  by  connecting  the  two 
ends  of  the  strip  to  suitable  recording  apparatus.  In  the  instance  of  a  wave 
of  contraction  which  passes  from  end  to  end  of  a  single  strip,  the  changes 
registered  are  diphasic  ;  for  at  first  the  excited  end  is  negative  to  the  distal 
end,  and  eventually,  as  the  distal  end  becomes  negative,  the  excited  end  is 
relatively  positive. 

Now  precisely  analogous  changes  in  electric  state  occur  in  visceral 
musculature,  such  as  cardiac  muscle,  contracting  under  the  influence  of 
physiological  impulses,  and  these  may  be  similarly  recorded.  Activity  is 
always  associated  with  the  development  of  negativity,  and  if  leads  are  made 
from  base  and  apex  of  the  ventricle  and  the  electric  state  of  one  relative  to  the 
other  is  recorded,  it  will  be  obvious  that  a  very  definite  idea  of  the  direction 
which  the  contraction-wave  takes  in  the  ventricle  may  be  formed.  And,  further, 
an  important  clue  to  the  point  at  which  contraction  starts  will  be  at  our  disposal. 
These  conclusions  are  of  great  importance,  and  should  form  the  basis  of  all 
electro-cardiographic  studies. 

2.  Electric  changes  as  a  residt  of  the  heart  beat. 

In  the  frog,  electric  changes  as  a  result  of  the  heart  beat  were  described 
by  Kolliker  and  Miiller^^^  in  1855  ;  their  observations  were  followed  by  those 
of  many  other  workers.  The  mammalian  heart  was  the  subject  of  special 
investigation  at  the  hands  of  Waller  *^''  '*^^'  *°^  and  others.  It  was  found  that 
the  type  of  curve  yielded  by  leads  from  base  and  apex,  is  approximately  dupH- 
cated  by  leads  from  other  parts  of  the  body.     Stated  in  a  simple  form,  it 

*  The  expenses  of  the  work,  upon  which  this  appendix  is  based,  have  been  defrayed  by 
the  British  Medical  Association. 


THE  ELECTRO-CARDIOGRAM 


371 


was  showTi  that  the  body  can  be  mapped  out  by  a  plane  crossing  the  base 
of  the  heart,  into  two  parts,  one  abutting  upon  the  base,  the  other  including 
the  apex  of  the  ventricle  ;  and  that  leads  from  these  tivo  divisions  of  the  body 
are  equivalent  to  leads  from  base  and  apex  of  the  ventricle.  Thus  the  possibihty 
of  registering  the  electric  changes  produced  by  the  heart  beat  in  the  intact 
animal  was  demonstrated,  and  in.  man  they  were  first  studied  by  Waller. 
In  the  human  subject,  the  dividing-Une  already  referred  to  passes,  according 
to  the  last-named  writer,  from  the  left  shoulder  to  the  right  loin.  The  right 
arm  may  therefore  be  utihzed  as  a  basal  lead,  while  the  left  arm,  or  either 
leg,*  serves  as  an  apical  lead.     Leading  off  from  the  human  body,  through 


Fig.  275,  for  which  we  are  indebted  to  Professor  Einthoven,  shows  a  portion  of  a  carotid 
curve  and  a  single  beat  of  an  electric  curve.  The  abscissae  are  divided  at  intervals  of 
0-01  sec. ;  the  ordinates  are  divided  at  intervals  of  10~*  volt.  The  lead,  as  in  all  figures 
shown,  was  from  right  hand  and  left  foot.  In  this,  as  in  all  figures  also,  corresponding  points 
of  time  are  directly  vertical  to  each  other,  p  represents  the  auricular  and  r,  s,  and  t  the 
ventricular  contraction. 

the  unbroken  skin,  records  of  the  electric  change  as  a  result  of  systole  of 
the  ventricle  may  therefore  be  obtained,  and  they  correspond  very  closely  to 
records  yielded  experimentally  by  direct  leads  from  base  and  apex  of  the 
mammalian  heart.  In  addition,  distinct  changes  as  a  result  of  auricular 
contraction  are  registered. 

The  method  employed  clinically. 

The  galvanometer  which  is  employed  chnically  is  that  invented  by 
Einthoven  **^'  ^^,  to  whose  papers  the  reader  is  referred  for  a  detailed 
account  of  its  construction  and  working. 

It  consists  of  a  heavy  magnet,  permanent  or  in  circuit,  the  poles  of  which 
are  close  together.  Between  the  poles  a  fine  platinum  or  silvered  quartz 
thread   is    suspended.     When    the    instrument  (string   galvanometer)  f   is 

*  The  changes  registered  necessarily  vary  to  some  extent  with  the  '  lead  '. 
t  Sold  by  the  Cambridge  Scientific  Instrument  Co.,  and  by  Dr.  Th.  Edelmann  of  Miinich. 

B  b  2 


372 


DISEASES  OF  THE  HEART 


working,  the  thread  Hes  in  a  powerful  magnetic  field,  and  deviates  whenever 
a  current  is  led  through  it.  The  shadow  of  the  string  and  its  movements  are 
magnified  and  projected,  by  means  of  a  system  of  lenses  and  an  arc  light,  on 
to  a  photographic  apparatus.  The  delicacy  of  the  instrument  depends 
upon  the  strength  of  the  magnetic  field,  and  the  fineness  of  the  conducting 
thread.  The  body-current  which  it  is  desired  to  register  is  led  from  the 
limbs  (right  arm  and  left  leg,  or  right  arm  and  left  arm)  by  immersing  them 
in  electrolytic  solutions  which  are  in  connexion  with  the  ends  of  the  suspended 
thread. 


S  S  S  S        ^/ect.       s 

Fig.  276.  Simultaneous  records  of  time,  in  ^  sec,  venous  and  electro-cardiographic 
curves.  The  delay  in  the  venous  curve  is  due  to  the  aii*  transmission  employed,  to  the 
delay  in  transmission  from  auricle  to  neck,  and  to  the  fact  that  the  electric  change  slightly 
precedes  the  contraction.  From  a  patient  in  which  the  p-r  and  a-c  intervals  show  sUght 
prolongation,  but  in  which  the  curve  is  otherwise  normal. 

3.  The  normal  electro-cardiogram  and  its  significance. 

The  normal  electro-cardiographic  curve  consists  of  three  negative  and 
usually  one  positive  wave  (directed  upward  and  downward  respectively  in 
the  accompanjdng  figures).  They  are  designated  by  the  letters  p,  r,  and  t 
(negative  peaks)  and  s  (positive  depression),  p  is  a  result  of  auricular 
contraction,     r,  s,  and  t  are  due  to  systole  of  the  ventricle. 

The  ventricular  portion  of  the  curve  (r,  s,  and  t)  is  thus  triphasic*     It 

*  Not  infrequently  the  curve  shows  four  phases,  q,  r,  s,  and  t  (Fig.  275).  The  depression 
Q,  which  is  distinct  in  Fig.  275,  is  usually  less  marked  than  the  depression  s,  but  may  be 
more  prominent  than  the  latter.  In  brief,  the  opening  events  of  the  ventricular  electro- 
cardiogram are  subject  to  variations,  and  it  is  possible  that  these  variations  depend  on  slight 
differences  in  the  direction  of  the  contraction- wave  when  it  starts  in  the  ventricular  muscula- 
ture. It  will  simplify  the  description  if  further  reference  to  tliis  depression  q  is  omitted,  for 
it  is  not  certain  that  it  is  ventriaular  in  origin.  Nevertheless,  its  frequent  presence  should 
not  be  forgotten. 


THE  ELECTRO-CARDIOGRAM  373 

shows  two  displacements,  r  and  t,  in  a  direction  indicating  negativity  of 
the  base  of  the  heart,  and  one  displacement,  s,  indicating  negativity  of 
the  apex  (or  positivity  of  the  base).  The  curve  is  of  such  a  nature  as  to 
suggest  that  the  contraction  of  the  heart  originates  at  its  base,  travels  to  the 
apex,  and  returns  to  the  base  (Gotch**")  (cf.  §  1). 

4.   Variations  in  the  individual  electro-cardiographic  curve. 

Both  auricular  and  ventricular  portions  of  the  galvanometer  curve  are 
subject  to  considerable  variation  in  form,  a  variation  seen  more  especially 
in  pathological  conditions.  Thus  in  mitral  stenosis  an  increase  in  the  size 
of  P  accompanies  hypertrophy  of  the  auricle,  and  in  the  later  stages  of  the 
affection,  p  shows  a  division  into  two  parts  (p^  and  P2  of  Fig.  277),  and  may 
be  prolonged  as  a  whole.  (The  normal  p-r  interval  varies  from  •12-- 16 
seconds  ;  the  p-r  interval  in  the  accompanying  figure.  Fig.  277,  is  -2  second  ; 
in  the  normal  curve,  Fig.  275,  it  is  -15  second). 


Fig.  277.     From  a  case  of  mitral  stenosis  and  aortic  regurgitation.     Showing  tlie  prolonga- 
tion of  P-R  interval,  a  splitting  of  p,  and  an  increase  in  s. 

Similarly,  variations  are  met  with  in  the  ventricular  portion  of  the  curve. 
Thus  hypertrophy  of  the  left  ventricle,  especially  hypertrophy  of  its  apical 
portions,  such  as  is  met  with  in  aortic  regurgitation,  is  commonly  accom- 
panied by  an  increase  in  the  magnitude  of  the  variation  s.  This  fact,  which 
is  in  accordance  with  the  interpretation  of  the  normal  curve,  is  well  illus- 
trated in  Fig.  277,  and  in  the  patient  from  which  this  curve  was  obtained 
left  ventricular  hypertrophy  was  a  notable  feature. 

5.  Analysis  of  the  sequence  of  contraction  in  the  cardiac  chambers. 

In  the  last  paragraph  examples  were  given  illustrative  of  information 
to  be  obtained  from  individual  auricular  or  ventricular  curves,  where  the 
heart  beat  shows  the  usual  sequence  of  chamber  contraction.  The  method 
is  of  still  greater  service  in  the  analysis  of  disordered  sequence,  and  in  this 
direction  forms  a  valuable  adjunct  to  venous  pulse  work. 

For  the  time  being  two  examples  will  suffice.  Fig.  278  is  taken  from 
a  case  of  complete  heart-block.     The  photograph,  as  a  whole,  is  composed 


374 


DISEASES  OF  THE  HEART 


of  frequent  auricular  and  infrequent  ventricular  curves,  accurately  super- 
imposed upon  each  other.  The  ventricular  curve  is  identified  by  the  peak  R, 
its  most  constant  feature.  The  variation  t  is  anomalous  and  inverted  (a  by 
no  means  uncommon  occurrence  in  pathological  conditions).  The  peak  p 
occurs  at  regular  intervals  in  the  figure,  and  whenever  it  falls  with  a  ven- 
tricular curve  it  is  superimposed  upon  it. 

The  second  example  is  shown  in  Fig.  279,  and  is  taken  from  a  patient 
with  the  disorderly  action  of  the  heart,  termed  '  Nodal  rhythm  '  in  this  book. 
It  shows  no  sign  of  the  normal  auricular  contraction  during  the  diastole  of 
the  heart.     Further,  it  shows  marked  tremulousness  of  the  line  joining  the 


Fig.  278.     From  a  case  of  complete  heart-block,  showing  the  dissocixtion  of   auricle  and 

ventricle. 


Fig.  279.     From  a  case  of  '  nodal  rhythm ',  showing  the  absence  of  the  normal  wave  p,  and 
the  presence  of  irregular  waves  having  fixed  relationsliip  to  other  events. 

peaks  R.  This  tremulousness  has  been  found  in  association  with  myocardial 
degeneration*  (Einthoven,  Kraus  and  Nicolai *^2» *^ ). 

6.  The  point  in  the  musculature  at  which  a  contraction  arises. 

In  the  preceding  paragraphs  the  importance  of  electro-cardiographic 
curves  have  been  shown  from  two  separate  aspects.  First,  they  give  infor- 
mation of  the  nature  of  a  contraction  in  auricle  or  ventricle  respectively. 
Secondly,  they  serve  in  the  analysis  of  disordered  rhythm  and  in  the  elucida- 
tion of  disturbed  sequence  of  systole.     Information  of  the  first  and  second 


*  The  explanation  of  the  tremulousness  will  be  fully  dealt  with  in  an  early  article  to 
Heart. 


THE  ELECTRO-CARDIOGRAM 


375 


order  is  also  obtained  by  other  methods ;  by  direct  inspection,  palpation  or 
percussion,  &c.,  and  by  means  of  graphic  records  from  pulsating  areas.  The 
electro-cardiogram  may  consequently  be  said  to  yield,  as  a  rule,  evidence 
which  is  but  confirmatory  of  that  obtained  by  other  means,  when  regarded 
from  these  special  points  of  view.  But  on  this  account  its  importance  should 
not  be  underrated,  for  it  frequently  happens  that  the  remaining  physical 
signs  are  obscure  or  difficult  to  obtain. 

Finally,  the  galvanometer  yields  evidence  of  a  distinctive  nature.  It 
allows  recognition  of  contractions  arising  in  the  separate  chambers  of  the 
heart,  which  start  in  areas  of  the  musculature  other  than  the  normal. 
It  is  in  this  direction  that  galvanometric  observations  promise  the  richest 
harvest  of  fact.     We  have  seen  that  the  normal  electro-cardiogram  of  the 


fl^F^^^^^^^^^^^'^^f^l^^P^lf^^f^^fP^IP^P^^fi^^ 


y^sec 


Fig.  280.  The  curve  shows  tliree  beats  in  which  the  normal  p-r  sequence  is  observed, 
and  four  extra-systoles  of  the  ventricle.  The  p  waves  which  are  regular  are  superimposed 
upon  the  extra-systoUc  curves  in  three  places  (dotted  Unes). 

ventricle  commences  with  a  taU  and  sharply-pointed  peak,  e,  and  it  has 
been  stated  that  in  the  presence  of  this  peak  we  have  presumptive  evidence 
of  the  origin  of  ventricular  contraction  in  the  morphological  base  of  the 
ventricle.  In  examples  of  complete  heart-block  (Fig.  278),  the  ventricular 
curve  commences  in  the  same  way,  and  we  may  conclude  with  a  fair  degree 
of  certainty  that  the  beats  of  the  ventricle  in  this  condition  are  propagated 
from  a  point  in  its  musculature,  corresponding  to  that  from  which  they  start 
in  the  normal  beat.  A  similar  observation  applies  to  the  curves  of  *  nodal 
rhythm  '  (Fig.  279).  In  this  instance,  as  in  that  of  complete  heart-block  also, 
it  may  be  asserted  that  all  the  beats  start  in  the  ventricle  from  a  single  focus. 
In  Fig.  280  an  example  of  ventricular  extra-systoles  is  portrayed.  The 
normal  beats  (of  which  three  are  present)  are  represented  by  p,  R 
variations.  The  extra-systohc  curves  (of  which  four  are  present)  are  highly 
atypical.     Each   is   manifested   by   a   primary  positive   and   a   secondary 


376  DISEASES  OF  THE  HEART 

negative  displacement.  They  are  all  of  the  same  nature,  and  therefore  arise 
from  a  single  focus  in  the  ventricular  musculature.  The  actual  point  of 
origin  is  undecided,  but  there  is  evidence  to  show  that  they  proceed  from 
the  left  ventricle  and  rather  from  its  apical  than  from  its  basal  portion.* 
*rhe  ultimate  elucidation  of  the  birth-place  of  anomalous  beats  of  a  nature 
similar  to  those  shown  is  a  matter  of  experiment  and  time.  It  will  be 
obvious  from  the  remarks  in  §  1  that  when  a  systole  of  the  ventricle  starts 
at  a  point  other  than  the  normal,  such  atjrpical  curves  must  result,  and  that 
many  forms  of  atypical  curve  are  to  be  anticipated.  Such  is  found  to  be 
the  case,  but  at  present  a  fuU  description  of  these  curves  would  not  be 
profitable.  Again,  just  as  beats,  arising  in  areas  of  the  ventricular  muscula- 
ture other  than  the  normal  starting-points,  produce  atypical  electrical 
curves,  so  also  do  those  beats  which  arise  out  of  place  in  the  auricle.  For 
example,  when  a  beat  of  the  auricle  is  started  by  a  beat  of  the  ventricle 
(retrograde  contraction)  the  peak  p  disappears  and  is  replaced  by  a  curve 
of  a  highly  atypical  character. 

The  importance  of  this  aspect  of  the  electro-cardiogram  will  now  be 
clear,  for  in  all  probability  it  will  eventually  be  possible  to  accurately 
determine  the  focus  in  which  the  impulses  of  all  such  abnormal  contractions 
are  developed. 

It  occasionally  happens  that  extra-systolic  contractions  of  the  ventricle 
fall  at  such  points  in  the  auricular  cycles  that  it  is  impossible  to  determine 
by  venous  pulse  methods  whether  such  ventricular  beats  are  the  result  of 
transmitted  auricular  impulses  or  not.  In  such  cases  the  nature  of  the 
electro-cardiographic  curve  of  these  beats  may  be  very  helpful.  In  Fig.  280 
the  second  auricular  curve  falls  upon  the  first  extra-systolic  curve  (it  is 
indicated  by  a  dotted  outUne).  It  is  succeeded  by  a  contraction  of  the 
ventricle,  which  in  the  absence  of  the  galvanometric  curve,  might  have  been 
readily  mistaken  for  a  response  to  auricle.  With  the  evidence  of  the  electric 
curve  before  us,  its  origin  in  an  auricular  impulse  can  be  definitely  denied, 
and  it  is  recognized  as  an  extra-systole  of  precisely  the  same  nature  as  those 
which  precede  and  succeed  it. 

*'  Curves  identical  with  those  shown  in  the  figure  may  be  obtained  by  electrical  stimulation 
of  the  heart  apex. 


Fio.  4.     Respiratory 


Fig,  5.     Respiratory  e 


from  B  case  of  Cbeyne-Stokea  respiration  (see  page  29). 


s  from  a  caae  of  Cheyne-Stokes  respiration  (see  page  29) 


1  and  the  radial  pulse  from 
le  in  the  radial  tracing  rises 
during  the  respiratory  phase  and  the  irregularity  of  the  pulse  (due  to  depression  of 
contractility)  becomes  more  marked.  The  blood  pressure  also  rose  at  the  same  time. 
(Case  23,  Appendix  V ;  see  page  29.) 


Fia.  7.     Tnicing  of  the  respiratory  movements  and  of  the 
during  Cheyne-Stokea  respiration  (see  page  30). 


due  to  Hiccough  (H) 


75.  Sinus  irregularity  produced  by  reflex  stimulation  o£  the  vagus  by  the  act  of 
swalloH-ing.  The  numbers  re'er  to  the  duration  of  each  cardiac  cycle  in  tenths  of 
seconds,  and  they  show  that  the  heart  quickened  its  rate  for  a  few  beate  after 
gwallowiog,  then  gradually  slowed ;  then  again  increased  slightly  io  rate,  followed 
by  another  short  period  ol  slowing  (9i  &  94).  The  respiratory  curve  shows  that  tlie 
irregularity  was  independent  of  respiration.  Compare  with  Figs.  258  and  259, 
Plate  IV  (see  page  144). 


IS)  shown  by  a  temporary 


o 


Fin.  "7.    The  respiratory  mov< 


I.     luc  respiratory  movomenM  vttre  «t  tho  rale  of  7  or  8  per  minute     There  Is 


i  patient  that  gave  Figs.  90  and  ] 


Fiu.  IM  is  from  tUe  t 

periods  during  which  the  large  bro 

was  due.     They  are  probably  tlie  result  of  pn 
o(  auriele  and  ventricle— being  therefore  nodal  i 


appear  before  the  a 


ira-systoles  during  A  and  D  (see  page  159), 


Flc.  too.    The  extra-syatolos  [a',  r')  arc  of  nodol  origin,  and  the  a-e  interval  after  the 
pauses  IS  ahortened  and  gradually  inoroases  in  length  (epacea  A,.  ,1,,  A^  A,) 


.    Simultaneous  tracings  of  Uio  apex  beat  and  the  radial  to  show 
e  page  320.) 


>  iiuuuigs  ui  uiB  apex  oeat  ana  tue  radial  to  show  the  irregularity 
the  Budden  inception  of  the  nodal  rhythm.     (Case  Hi,  July.  1900  ; 


C) 


I 


IlG. 


Fig. 


Fig. 


Fig. 


Fio.  200.     Shows  the  charnclcristic  change  in  the  jugular  pulso  (venlrtcular  form  of  jugi 

pulse)  with  " ■'■''-  ' "  -    -'  ■'  ..... 

page  320). 


pulse)  with  the  sudden  iacoption  of  the  noi^  rhythm.     (Case  10.  July. 


slower,   the  irreguJarity  and  jugular  pulse 


Ro.  238.     Continued  iiTC^arily   which   has  porabted  fiom   1004    to    IU08.     The  jugulai 
pulse  ia  ol  the  vcnUiDuIar  form.     {Case  17,  190S ;  sec  page  340.) 


■8  tl)e  pulsus  ^iltcrnanH  in  the  radial  tracings  with  tlic  frequent  occurrence  c 
,r  cxtra-syslolcs  (r').  In  the  jugular  tracing  there  is  only  one  large  wave,  . 
.  „....;„i»     rru ^  impairment  of  conductivity  ol  the  a-v  biuidlo.  i 


ludle,  and  of  deptc&scd  conlractiUty 


o 


Fio.  244.     The  respirnto 


of  the  pulsus  altenmna.     (Case  24 


Shovrs  a  reflex  effect  of  the  vagus  d 
e  diagram  in  Pig.  2o9).     After  this  tl 


hcort'a  irregularity 
ince  of  the  ra<"'  ' 

lystoles  (r")  and  ai 


radial  pulae 
page  354.) 


1  be  independent  of  the 
I,  after  the  smaller 


§walloning.  After  the  act  of  avallotring 
dropping  out  uf  the  ventricular  syatoles 
art's  rate  increased  slightly,  then  became 


Piti,  iW.    ShowR  the  same  na  Fig.  2S8,  except  that  during  the  second  period  of  stoning  aftej 
nivalloH-ing  there  is  n  long  paiue  due  to  the  dropping  out  of  a '     '  '   "    ' 


Fio,  201.    Shan's  the  inocptJon  of  the  nodal  rhythm  aft«r  digitalis.    Compare 
pulse  and  the  niurmuiB  with  Fig.  212.  page  305.     (Case  OS  ;  see  page  360, 


Fio.  203,    Shows  the  arrest  of  the  whole  heart  for  1 

Fig.  273.  page  307-     Digila  Us  effect.     tCa«e28;  seepage  360.) 


^KJVJ\rJVJVJ\/^-^^ 


o 


w 


205.  Slowing  of  the 
of  the  0-1.  bundle 
approached  t 

shown  by  tbe  eboding.    (d'os 


Rq.  200,     Extra-ayatoles,  r'.  probably  of 

are  due  to  the  extra- systole.     Tliere  ore  occi 
occurred,  followed  by  a  shortening  of  tbe  a-e 


bole  heart  due  to  digitalis.     During  tbe  pauses  the  conductivity 

"" -"   "-■    -'         incular  wave  a   griidunlly 

The  murmur  due  to  the 
med  to  become  lost  in  the  tirst  sound,  as 


gin.  due  to  digitalis.    The  waves  v' 
I  long  pauses  when  no  extra-eystole 


Q  of  Fig.  200  and  shows  the  same  kinda  of  irregularity.    (Coae  28 ; 


•  irregularity  und  ventricular  form  of  ■ 
which  linally  became  pennaDcnt  i 

t 


c 


BIBLIOGEAPHY 

The  bibliography  given  here  deals  mainly  with  articles  bearing  on  the  more  recent  inquiries 
into  cardiac  symptoms.  As  my  own  views  are  sufficiently  expressed  in  the  text  I  have  given 
references  to  only  a  few  of  my  own  articles,  except  in  the  case  of  those  dealing  •with  the  sensory 
or  reflex  phenomena  of  visceral  disease,  and  on  this  subject  fairly  full  references  are  given, 
as  I  am  deeply  impressed  with  the  importance  of  this  subject  in  its  relation  not  only  to  cUnical 
medicine,  but  also  to  clinical  surgery,  and  consider  that  the  profession  in  general,  and  clinical 
teachers  in  particular,  have  not  fully  realized  the  significance  of  this  class  of  symptom. 

I.    ANGINA  PECTORIS  AND  SENSORY  SY:MPT0MS  ASSOCIATED  WITH 

VISCERAL  DISEASE 

1.  Allbtttt.    On  Visceral  Neuroses.    The  Gulstonian  Lectures  for  1884.    London,  1884,  p.  31. 

2.  Broadbent.    Heart  Disease,  4th  Edition. 

3.  Brodie.    Recent  Work  on  Visceral  and  allied  Nerves.    Science  Progress,  1896,  No.  1. 

4.  Brtjnton.    Nitrite  of  amyl  in  Angina  Pectoris.    Chnic.  Soc.  Rep.,  vol.  iii,  1870. 

5.  Charante.    De  Hyperalgetische  Zonen  van  Head.    Leiden,  1900. 

6.  Garrod.     Angina  Pectoris  due  to  plugging  of  the  coronary  artery.    Proc.  Roy.  Soc.  of 

Med.,  April,  1908. 

7.  Gaskell.     On  the  structure,  distribution,  and  functions  of  the  nerves  which  innervate 

the  viscera  and  vascular  system.    Jom-n.  of  Physiol.,  vol.  vii,  1886,  p.  1. 

8.  Gibson.    Nervous  Affections  of  the  Heart,  1904. 

9.  Some  hitherto  undescribed  symptoms  in  Angina  Pectoris.    Brain,  1905,  part  cix. 

10.  Haller.     '  De  partibus  c.h.  sensibiUbus  et  irritabiUbus.'    Gottingen,  1752. 

11.  Hare.    The  Food  Factor  in  Disease.    1905. 

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Brain,  vol.  xvi,  p.  1. 
14. Ibid.    Part  II :  Head  and  Neck,  vol.  xvii,  p.  339. 

15.  Ibid.    Part  III :   Heart  and  Lungs,  vol.  xix,  p.  153. 

16.  The  afferent  nervous  system  from  a  new  point.    Brain,  vol.  xxvii,  p.  99. 

17.  Head  and  Sherren.     The  consequences  of  injury  to  the    peripheral  nerves  in  man. 

Brain,  vol.  xxviii,  p.  116. 

18.  Head   and  Thompson.    The  grouping    of   afferent  impulses   witliin  the  spinal  cord. 

Brain,  vol.  xxix,  p.  537. 

19.  Head  and  Campbell.    The  pathology  of  herpes  zoster  and  its  bearing  on  sensory  localisa- 

tion.   Brain,  vol.  xxiii,  p.  353. 

20.  Heitz,    Les  Nerfs  du  Coeur  chez  les  Tabetiques.    Paris,  1903. 

21.  Herringham.     The  minute  anatomy  of  the  brachial  plexus.     Proc.  of  the  Roy.  Soc, 

vol.  xU,  1887,  p.  423. 

22.  Hertz,  Cook  and  Schlesinger.    The  sensibility  of  the  stomach  and  intestines  in  man. 

Journ.  of  Phys.,  vol.  xxxvii,  December,  1908. 

23.  Hoffmann.    Pathologie  und  Therapie  der  Herzneurosen.    Wiesbaden,  1901. 


378  DISEASES  OF  THE  HEART 

24.  loTEYKO.    Le  sens  de  la  Douleur.    Journal  de  Neurologie,  October,  1905. 

25.  Kart  and  Meltzer.    Die  Sensibilitat  der  Bauchorgane.    Mitteilungen  aus  den  Grenz- 

gebieten  der  Med.  u.  Chir.,  vol,  xix,  p.  586. 

26.  Langley.    The  autonomic  nervous  system.    Brain,  Part  I,  1903, 

27.  Lennander,    Observations   on    the   Sensibility    of   the   Abdominal   Cavity,      Barker's 

translation,  1903. 

28.  JIackenzie.    Symptoms  and  their  interpretation.    London,  1909. 

29. Contribution  to  the  study  of  sensory  symptoms  associated  with  visceral  disease. 

Medical  Chronicle,  August,  1892. 
30. Some  points  bearing  on  the  association  of  sensory  disorders  and  visceral  disease. 

Brain,  Ixiii,  1893. 

31.  The  '  pilomotor  '  or  '  goose-skin  reflex  '.    Brain,  Ixiv,  1893, 

32.  Heart  pain,  and  sensory  disorders  associated  with  heart  failure.    Lancet,  January  5, 

1895. 

33.  Pain.    Brain,  xcix,  1902. 

34, Article, '  Visceral  Pain.'    Encycl.  Medic.  Edinburgh,  1902. 

35, A  suggestion  for  the  observation  of  new  paths  in  the  spinal  cord.     Caledonian 

Medical  Journ.,  April,  1905. 
36. The  meaning  and  mechanism  of  visceral  pain.    Brit.  Med.  Journ.,  June,  1906. 

37.  An  inquiry  into  the  cause  of  Angina  Pectoris.    Brit.  Med.  Journ.,  October  7, 

1905. 

38.  Murray.    Diagnosis  and  treatment  based  on  visceral  reflexes.    Univ.  Penn.  Med.  Bull., 

May,  1908,  p.  71. 

39.  Nothnaqel.    Angina  Pectoris  vaso-motoria.    Deutsches  Archiv  f.  khn.  Med.  Leipzig,  1867. 

40.  Schmerzhafte    Empfindungen    bei  Herzerkrankungen,     Zeitsch,    f.    klin,    Med. 

Berhn,  1891. 

41.  OsLER.    The  Principle  and  Practice  of  Medicine,  6th  Edition. 

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korperchen  im  Peritoneum  parietale  des  Menschen.     Anatomische  Hefte.     Heft  109, 
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p.  613. 

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having  its  origin  in  the  Abdomen.    Brit.  Med.  Journ.,  February  10,  1906. 

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sklerose  und  sonstige  Erkrankungen  der  linksseitigen  Herzhalfte.    Miinchener  Med. 
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48.  Sherrington,    Article,  '  Cutaneous  sensations,'  Schaefer's  Text  Book  of  Physiology. 

49.  The  Integrative  Action  of  the  Nervous  System.    London,  1906. 

50. Peripheral  distribution  of  the  fibres  of  the  posterior  roots  of  some  spinal  nerves. 

Phil.  Trans.  Roy.  Soc,  London,  vol.  cxc,  p.  45. 

51.  Steell.    Textbook  on  Diseases  of  the  Heart,  1906. 

52.  Sturge.     The  phenomena  of  Angina  Pectoris   and    their  bearing   upon  the   theory  of 

counter-irritation.    Brain,  vol.  v,  1883,  p.  492. 

53.  Trotter  and  Davies.    The  exact  determination  of  areas  of  altered  sensibility.    Rev.  of 

Neurol,  and  Psychiat.,  October,  1907. 
54. Experimental  studies  in  the  innervation  of  the  skin.    Journ.  of  Physiol.,  vol.  xxxviii, 

February,  1909. 
55.  Weber.    Case  of  Angina  Pectoris  with  Aortitis.    Proc.  Roy.  Soc.  of  Med.,  April,  1908. 


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Lancet,  April  16,  1904. 

57.  Wilson.    The  onset  of  fear  and  the  onset  of  pain  in  cardiac  disturbance.    Trans.  Med. 

Ch.  Soc.  of  Edinburgh,  1905. 


II.    BLOOD  PRESSURE 

58.  Allbutt.    Clinical  remarks  on  Arterio-sclerosis.    Brit.  Med.  Journ.,  October  20,  1906. 

59.  The  senile  cardio-vascular  system.    The  Hospital,  November  16,  1907. 

60.  Basch.    Ueber  die  Messung  des  Blutdrucks  am  Menschen.    Zeits.  f.  klin.  Med.,  1881. 

61.  Broadbent.     Clinical  significances  and  therapeutical  indications  of  variations  in  the 

blood  pressure.    Brit.  Med.  Journ.,  October  20,  1906. 

62.  Dawson.      The  lateral  blood  pressure  at  different  points  of  the  arterial  tree.      Amer. 

Journ.  of  Phys.,  1906,  vol.  xv. 

63.  The  systohc  output  and  work  of  the  heart  and  their  relation  to  the  blood  pressure 

in  man.    Brit.  Med.  Journ.,  October  20,  1906. 

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continuous  irregularity  of  the  Heart.    Brit.  Med.  Journ.,  March  5,  1904. 

212.  MacWilliam.    On  the  influence  exercised  by  the  central  nervous  system  on  the  cardiac 

rhythm.    Proc.  Roy.  Soc,  vol.  liii. 

213.  MusKENS.     An  analysis  of  the  action  of  the  vagus  nerve  on  the  heart.     Amer.  Jom-n. 

Phys.,  1898. 

214.  Nicholson.    Article,  '  The  pulse,'  Encycl.  Med.    Edin.,  1902. 

215.  Pan.    Ueber  das  Verhalten  des  Venenpulses  bei  den  dm-ch  Extrasystolen  verursachten 

Unregelmassigkeiten  des  menschhchen  Herzens.     Zeitsch.  f.  exp.  Path,  und  Ther., 
Bd.  i. 

216. Klinische  Beobachtung  iiber  ventriculare  Extrasystolen  ohne  kompensatorische 

Pause.    Deut.  Arch.  f.  kUn.  Med.,  Bd.  Ixxviii. 

217.  Polimanti.    Sur  I'allorythmie  du  coeur.    Journ.  de  Phys.  et  de  Path,  gen.,  septembre 

1906. 

218.  Ratjtenberg.    Die  Analyse  der  Extrasystolen  im  Bilde  der  Vorhofpulsation.    Miinch. 

Med.  Woch.,  No.  50,  1907. 

219.  Reissner.     Ueber  unregelmassige  Herzthatigkeit  auf  psychischer  Grundlage.     Zeitsch. 

f.  kUn.  Med.,  Band  liii. 

220.  Riegel.     Zur  Lehre  von  der  Herzirregularitiit  und  Incongruenz  in  der  Thiitigkeit  der 

beiden  Herzhalften.    Wiesbaden,  1891. 

221.  RiHL.     Experimentelle  Analyse  des  Venenpulses  bei  den  durch  Extrasystolen  verur- 

sachten Unregelmassigkeiten  des  Saugethierherzens.     Zeitsch.   f.   exp.  Path,   und 
Ther.,  Band  i. 
222. Ueber  Herzalternanz  beim  Menschen.    Zeitsch.  f.  exp.  Path,  und  Ther.,  Bd.  iii. 


BIBLIOGRAPHY  385 

223.  Ritchie.    The  Differentiation  of  the  varieties  of  extra-systole.    The  Scottish  Med.  and 

Surg.  Journ.,  June,  1907. 

224.  Salaghi.      Ueber  die  Herzarhytlimie   der   Rekonvaleszenten.      Monatsch.    f.   Kinder- 

heilkunde,  April  1904. 

225. Ueber  den  Einfluss  der  Herzbigeminie  auf  die  Blutciiculation.     Arch.  f.  exp. 

Path,  und  Pharmak.,  Bd.  li. 

226.  VoLHARD.     Ueber  die  Pulsus  alternans  und  pseudoalternans.     Miinch.   Med.   Woch., 

No.  13,  1905. 

227.  — ■ Ueber  ventriculiire  Bigimonie  ohne  compensatorische  Paase  durch  riicklaufige 

Herzcontractionen.    Zeitsch.  f.  klin.  Med.,  Band  liii. 

228.  Wenckebach.    Ai-rhythmia  of  the  Heart.    Snowball's  Translation. 

229. Les  irregularites  du  coeur.     Ar?h.  des  ^Maladies  du  Coeur,  fevrier  1908. 

230.  Williams,  P.  W.     Effects  of  respiration  on  the  circulation  and  the  pulsus  inspirationi 
intermittens  vel  pulsus  paradoxus.     Brit.  Med.  Journ.,  August  17,  1907. 


VIII.    PAROXYSMAL  TACHYCARDIA 

231.  Allbutt.    System  of  Medicine,  vol.  v. 

232.  Balfour.     The  Senile  Heart,  1894. 

233.  Barr.    a  chnical  lecture  on  Paroxysmal  Tachycardia.    Brit.  Med.  Journ.,  July  16,  1904. 

234.  Bramwell.    Clinical  Studies.    April  1,  1905,  p.  298. 

235.  Cotton.     Notes  and  observations  upon  a  case  of  unusually  rapid  action  of  the  heart. 

Brit.  Med.  Journ.,  1867,  vol.  i,  p.  629,  and  1869,  vol.  ii,  p.  4. 

236.  Cowan,  Macdonald,  and  Binning.     The  venous  pulse  in  paroxysmal  tachycardia. 

Quart.  Jomn.  of  Medicine,  vol.  ii,  January,  1909,  p.  213. 

237.  CusHNY  AND  Edmunds.    Paroxysmal  irregularity  of  the  heart  and  auricular  fibrillation. 

Studies  in  Pathology.    Quatercentenary  of  the  University  of  Aberdeen,  1906. 

238.  Edmunds.    Unusually  rapid  action  of  the  heart.    Brit.  Med.  Journ.,  1867,  vol.  i,  p.  72L 

239.  Gibson.    Nervous  Affection  of  the  Heart,  1904. 

240.  Gill.     A  case  of  arrhythmia  of  the  heart.     Australasian  Med.  Gazette,  February  20, 

1908. 

241.  Hay.    Paroxysmal  Tachycardia.    Edin.  Med.  Journ.,  Januarj%  1907. 

242.  Herringham.    Concerning  paroxysmal  Tachycardia.    Edin.  Med.  Journ.,  1897,  p.  366. 
^43.  Hertz  and  Goodhart.    The  speed  hmit  of  the  human  heart.    Quart.  Journ.  of  Medicine, 

vol.  ii,  January,  1909,  p.  213. 

244.  Hewlett.     Doubling  of  the  cardiac  rhythm  and  its  relationship  to  paroxysmal  Tachy- 

cardia.   Journ.  Amer.  Med.  Assoc,  1906,  p.  941. 

245.  Hirschfelder.     Observations  on  a  case  of  palpitation  of  the  heart.     Johns  Hopkins 

Hospital  Bull.,  1906. 
246. ■  Observations  upon  paroxysmal  Tachycardia.     Johns  Hopkins  Hospital  Bull., 

October,  1906. 
247. Contributions  to  the  study  of   auricular   fibrillation,  paroxysmal  tachycardia, 

&c.    Johns  Hopkins  Hosp.  Bull.,  November,  1908. 
248.  Hoffmann.    Neue  Beobachtungen  liber  Herzjagen.    Deut.  Arch.  f.  khn.  Med.,  Bd.  Ixxviii. 

249. Ueber  Verdoppelung  der  Herzfrequenz  &c.    Zeitsch.  f.  klin.  Med.,  Band  hii. 

250. Pathologic  und  Therapie  der  Herzneurosen.    Wiesbaden,  1901. 

251.  Lewis.    Paroxysmal  Tachycardia.    Heart,  vol.  i,  1909. 

252.  OsLER.    The  Principles  and  Practice  of  Medicine,  6th  Ed. 

253.  ScHJiOLL.     Paroxysmale  Tachykardie.     Deut.  Arch.  f.  klin.  Med.,  Band  Ixxxix. 

254.  Watson.     On  a  case  of  unusually  rapid  action  of  the  heart.     Brit.  Med.  Journ.,  1867, 

vol.  i,  p.  752. 

MACKEKZIE  Q   Q 


386  DISEASES  OF  THE  HEART 

IX.    PRIMITIVE  CARDIAC  TISSUE,  HEART-BLOCK,  AND  ADA3IS-ST0KES 

SYNDROME 

(References  to  published  cases  with  post-mortem  reports  of  heart-block  will  be  found  in 
Lewis,  309.) 

255.  Adams.    Cases  of  diseases  of  the  heart.    Dublin  Hospital  Reports,  iv,  1827,  p.  396. 

256.  AscHOFF.    A  discussion  on  some  aspects  of  heart-block.    Brit.  Med.  Journ.,  October  27, 

1906. 

257.  Babr.    Case  of  Stokes-Adams  disease.    Brit.  Med.  Journ.,  October  27,  1906. 

258.  Barringer.     Report  of  a  case  of  Stokes- Adams  disease.     Arch.  Int.  Medicine,  vol.  iv, 

August,  1909,  p.  186. 

259.  Beards.    A  case  showing  the  Stokes- Adams  phenomena.    Brit.  Med.  Joiu-n.,  October  19, 

1907. 

260.  BONNIGER.     Ueber  einige  Falle  von  gestorter  Leitung  zwischen  Atrium  und  Ventrikel 

beim  kranken  menschlichen  Herzen.    Zeitsch.  f.  exp.  Path,  und  Therap.,  Bd.  i. 

261.  Braeunig.     Ueber  musculose  Verbindungen  zwischen  Vorkammer  und  Kammer  bei 

verschiedenen  Wirbelthierherzen.    Arch.  f.  Phys.,  1904,  Suppl.  i. 

262.  Bramwell.    A  case  of  Heart-block  with  fibrous  changes  and  partial  obliteration  of  the 

bundle  of  His.    Brit.  Med.  Jomn.,  1909,  i,  p.  995. 

263.  Chapman.    A  case  of  cardiac  Syphiloma  with  Bradycardia  and  obstruction  of  the  inferior 

Vena  Cava.    Lancet,  July  28,  1906. 

264.  Chatjveau.     L'intersystole  du  coeur.     Journ.  de  Phys.  et  de  Path,  gen.,  no.  1,  Janvier 

1900. 

265. De  la  dissociation  du  rhythme  auriculaire  et  du  rhythme  ventriculaire.    Rev.  de 

Men.,  Paris,  1885,  p.  161. 

266.  CoHN.    The  auriculo-nodal  junction.    Heart,  vol.  i,  1909. 

267.  Deneke.      Die    Uberleitungsstorungen   zwischen   Vorhof   und   Kammer   des   Herzens. 

Jahrbiicher  der  Hamb.  Staatskrankenanstalten,  xi,  2. 
268. Zur  Rontgendiagnostik   seltener    Herzleiden.     Deutsch.   Arch.    f.   klin.    Med., 

Bd.  Ixxxiv. 
269.  Erlanger.       Physiology  of  heart-block  in  mammals  with  especial  refei'ence  to  the 

causation  of  Stokes- Adams  disease.    Journ.  Exp.  Med.,  1906,  vol.  viii,  p.  8. 
270. Fiuther  studies  in  the  physiology  of  heart-block.     Amer.   Jotu-n.    of  Phys., 

Slay  1,  1906. 
27L A  review  of  the  physiology  of  heart-block  in  mammals.     Brit.  Med.  Journ., 

October  27,  1906. 

272. Experimental  Heart-block.    Heart,  vol.  i,  1909. 

273.  Erlanger  and  Hirschfelder.     Further  studies  on  the  physiology  of  heart-block  in 

mammals.     Amer.  Joru-n.  of  Phys.,  1903,  vol.  xv,  p.  153. 
274. Eine  vorlaufige  JNIitteilung  iiber  weitere  Studien  in  bezug  auf  den  Herzblock  in 

Saugetieren.    Zentralblatt  fiir  Physiologic,  Bd.  xix.  No.  9. 

275.  Finny.    Bradycardia    with    Arrhythmia    and    epileptiform    seizures.      Dublin    Jom-n. 

Med.  Sc,  May,  1906. 

276.  Galabin.     On   the   interpretation    of    cardiographic    tracings,    &c.      Guy's    Hospital 

Reports,  1875,  vol.  xx,  p.  261. 

277.  Gibson,  A.    The  heart  in  a  case  of  Stokes-Adams  disease.    Quart.  Journ.  Med.,  January, 

1908. 

278.  Gibson,  G.    Bradycardia.    Edin.  Med.  Journ.,  July,  1905. 

279. The  electromotive  changes  in  heart-block.    Brit.  Med.  Jomn.,  July  7,  1906. 

280. Heart-block.    Brit.  Med.  Journ.,  October  7,  1906. 


BIBLIOGRAPHY  387 

281.  Gibson  and  Ritchie.    Further  observations  on  heart-block.    Practitioner,  May,  1907. 

282. A  historic  instance  of  the  Adams-Stokes  Syndrome  due  to  Heart-block.     Edin. 

Med.  Journ.,  June,  1909. 

283.  Gillies.    A  case  of  Bradycardia.    AustraHan  Med.  Gaz.,  January  20,  1906. 

284.  GossAGE.    Cases  of  Stokes- Adams  disease.    CHn.  Soc.  Trans.,  vol.  xxxviii. 
285. —  Some  cases  of  partial  heart-block.    Clin.  Soc.  Trans.,  vol.  xl. 

286.  Handfobd.     Remarks  on  a  case  of  Gummata  of  the  heart.     Death  from  heart-block  ; 

rhythmical  contraction  of  the  auricles  during  the  long  pauses.     Brit.  Med.  Journ., 
vol.  ii,  1904. 

287.  Hay.    The  pathology  of  Bradycardia.    Brit.  Med.  Journ.,  October  21,  1905. 
288. Bradycardia  and  cardiac  arrythmia.    Lancet,  January  20,  1906. 

289. Heart-block  in  its  relationship  to  Stokes- Adams  disease.    Med.  Chron.,  September, 

1906. 
290. Stokes- Adams  disease.     Report  of    a  case.      Liverpool  Medico-Chir.  Journ., 

July,  1906. 

291.  Hay  and  Moore.    Stokes- Adams  disease  and  cardiac  arrythmia.    Lancet,  November  10, 

1906. 

292.  Hering.    Ueber  die  Erregungsleitung  zwischen  Vorkammer  und  Kammer  des  Saugethier- 

herzens,  &c.    Arch.  f.  die  ges.  Phys.,  Bd.  cvii. 
293. Nachvveis  dass  das  His'sche  Uebergangsbiindel  Vorhof  und  Kammer  des  Sauge- 

thierherzens  functionell  verbindet.    Arch.  f.  die  ges.  Phys.,  Bd.  cviii. 
294. Ueber  die  unmittelbare  Wirkung  des  Accelerans  und  Vagus  auf  automatisch 

schlagende  Abschnitte  des  Saugethierherzens.    Pfliig.  Arch.,  1905,  vol.  cviii,  p.  281. 
295. ijberleitungsstorungen  am  Saugethierherzen  mit  zeitweiligem  Vorhof systolenaus- 

fall.    Zeitschrift  flir  exper.  Path,  und  Therapie,  Berlin,  1906. 
296.  His,  Jr.     Dritter  intern.  Physiol.  Congress  in  Bern.     Centbl.  f.  Physiol.,  1895,  vol.  ix, 

p.  469. 
297. Ein  Fail  von  Adams-Stokes'scher  Klrankheit  mit  ungleichzeitigem  Schlagen 

der  Vorhofe  und  Herzkammern  (Herzblock).     Deutsch.  Arch.  f.  klin.  Med.,  1899, 

Ixiv,  p.  316. 

298.  HoLST.    Om  Stokes- Adams  sygdom  og  '  Heart-block  '  hos  menneskit.    Kristiania,  1908- 

299.  HuMBLET.    Le  faisceau  interauriculo-ventriculaire  constitue  le  lien  physiologique  entre 

les  oreillettes  et  les  ventricules  du   coeur  du   chien.     Arch,  inter,  d.  Phys.,  1904, 
vol.  i,  p.  278. 
300. Allorhythme  cardiaque  par  section  du  faisceau  de  His.    Ibid.,  1906,  vol.  iii,  p.  330. 

301.  Jellinek  and  Cooper.    Report,  with  comment,  on  six  cases  of  heart-block  with  tracings 

and  one  post-mortem  examination  of  the  heart.    Brit.  Med.  Journ.,  Apr.  4,  1908. 

302.  Keith.    The  auriculo-ventricular  bundle.    London  Hosp.  Gaz.,  June,  1906. 

303.  Keith  and  Flack.     The  auriculo-ventricular  bundle  of  the  human  heart.     Lancet, 

August  11,  1906. 

304.  Keith  and  Miller.     Description  of  a  heart  showing  gummatous  infiltration  of  the 

auriculo-ventricular  bundle.    Lancet,  1906,  vol.  ii. 

305.  Kent.     Researches  on  the  structure  and  function  of  the  mammalian  heart.    Journ.  of 

Phys.,  1893,  vol.  xiv,  p.  233. 

306.  Kraus.     Einiges  iiber  functionelle  Herzdiagnose.     Deutsch.  Med.  Woch.,  1905,  pp.  1 

and  53. 

307.  Laslett.    a  case  exhibiting  the  Adams-Stokes  syndrome.    Lancet,  June  4,  1904. 

308. Syncopal  attacks  associated  with  prolonged  arrest  of  the  whole  heart.     Quart. 

Journ.  of  Medicine,  vol.  ii,  p.  347,  1909. 
309.  Lewis.     The  occurrence  of  heart-block  in  man  and  its  causation.     Brit.  Med.  Journ., 

vol.  ii,  1908,  p.  1798. 

C  c  2 


388  DISEASES  OF  THE  HEART 

310.  LoHMANN.    Zur  Automatie  der  Briickenfasern  und  der  Ventrikel  des  Herzens.    Physiol. 

Abtlieilung  des  Arch.  f.  Anat.  und  Physiol.,  Leipzig,  1904.    Bd.  i  und  ii. 

311.  Mackenzie.    Nodal  Bradycardia.    Heart,  vol.  i,  p.  23. 

312.  MONCKEBERG.      Untersuchungen    iiber    das    Atrioventricularbiindel    im    menschlichen 

Herzen.    Jena,  1908. 

313.  Morrow.    Heart-block.    Brit.  Med.  Journ.,  October  27,  1906. 

314.  Nagayo.     Pathologisch-anatomische     Beitrage    zum    Adams-Stokes" schen    Symptom- 

complex.     Zeitsch.  f.  klin.  Medizin,  67.  Bd.,  Hefte  5-6. 
316.  OsLER.     On  the  so-called  Stokes- Adams  disease.    Lancet,  August  22,  1903. 

316.  Retzer.      Ueber    die    musculose    Verbindung    zwischen    Vorhof    und    Ventrikel    des 

Saugethierherzens.    Arch.  f.  Anat.,  1904,  p.  1. 

317.  RiHL.     Analyse  von  fiinf  Fallen  von  Ueberleitungsstorungen.     Zeits.  f.  exp.  Path.  u. 

Therap.,  1905-6,  vol.  ii,  p.  82. 

318.  Ritchie.     Complete  heart-block  Avith  dissociation  of  the  action  of  the  amides  and 

ventricles.    Proc.  Roy.  Soc.  of  Edinbm-gh,  vol.  xxv.  Part  xii, 

319.  ScHMOLL.     Zwei  Falle  von  Adams-Stokes'scher  I^o-ankheit  mit  Dissociation  von  Vorhof 

und  Kammerrhythmus  und  LJision  des  His'schen  Biindels.    Deuts.  Arch.  f.  klin.  Med., 
Band  Ixxxvii. 
320. Adams-Stokes  disease.     Journ.  Amer.  Med.  Assoc,  vol.  xlvi,  p.  361. 

321.  Stengel.     Fatal  case  of  Stokes-Adams  disease  with  autopsy.     Amer.  Journ.  Med.  Sc, 

1905,  vol.  cxxx,  p.  1083. 

322.  Stokes.    Observations  on  some  cases  of  permanently  slow  pulse.    Dublin  Quart.  Journ. 

Med.  Sc,  1846. 

323.  Tawara.     Das  Reizleitungssystem  des  Saugethierherzens.     Jena,  1906. 

324.  Tigerstedt.     Ueber  die  Bedeutung  der  Vorhofe  fiir  die  Rhythmik  der  Ventrikel  des 

Saugethierherzens.    Arch.  f.  Physiol.,  1884,  p.  497. 

325.  Vaquez  et  Esmein.     Pouls  lent  d'origine  myocarditique  (Herzblock).     Bulletins  et 

Memoires  de  la  Societe  medicale  des  Hopitaux  de  Paris  (Seance  du  25  janv.  1907). 

326.  Webster.    Cardiac  Arrhythmia  in  relation  to  cerebral  anaemia  and  epileptiform  crises. 

Glasgow  Hospital  Reports,  1901. 

327.  Wenckebach.      Beitrage   zui-   Kenntniss   der    menschlichen   Herztatigkeit.      Arch.    f. 

Anatomic  und  Physiol.,  1906  and  1907. 
328. Arrythmia  of  the  Heart  (Snowball's  Translation). 

329.  Wilson.  The  nerves  of  the  atrio-ventricular  bundle.  Proc.  Roy.  Soc,  B,  vol.  Ixxxi,  1909. 

330.  WooLDRiDGE.     Ueber  die  Function  der  Kammernerven  des  Saugethierherzens.     Arch. 

f.  Physiol.,  1883,  p.  522. 

X.    TRICUSPID  REGURGITATION 

331.  Adams.    Dublin  Hospital  Reports,  1827,  vol.  iv,  p.  437. 

332.  Bramwell.    Diseases  of  the  Heart,  p.  531. 

333.  Fran(^ois-Franck.    Note  sur  la  reproduction  experimentale  des  insuffisances  valvulaires 

du  coeur.    Memoires  et  Bulletins  de  la  Societe  de  Medecine  de  Bordeaux,  (1882)  1883. 

334.  Gairdner.     On  the  action  of  the  auriculo-ventricular  valves  of  the  heart.     Dublin 

Hospital  Gazette,  October,  1857,  p.  295. 

335.  Gibson,  G.    Jugular  reflux  and  tricuspid  regurgitation.    Edin.  Med.  Journ.,  May,  1880, 

vol.  xxv. 
336. Our  debt  to  Ireland  in  the  study  of  the  circulation.    Dublin  Journ.  of  Medical 

Science,  1907. 
337.  Hebing.      Zur   experimentellen   Analyse   der   Um-egelmassigkeiten   des    Herzschlages. 

Separatabdruck  aus  dem  Archiv  fiir  die  ges.  Physiol.,  Bd.  Ixxxii,  Seite  8. 


BIBLIOGRAPHY  389 

338.  Hu>'TER.    Works,  Palmer's  Edition,  1835,  vol.  iii. 

339.  King.     The  safety-valve  function  in  the  right  ventricle  of  the  human  heart.     Guy's 

Hospital  Reports,  1837,  vol.  ii,  p.  132. 

340.  Luton.     Article  '  Circulation '  in  the  Nouveau  Dictionnaire  de  Medecine  et  Chirurgie 

pratiques,  tome  vii,  p.  715. 
3-41.  Mayo.    Outlines  of  Physiology,  4th  Edition,  pp.  44,  837. 

342.  Paton.     The  action  of  the  valves  of  the  mammalian  heart.     Trans.  Roy.  Soc.  Edin., 

vol.  xxxvii,  Part  1  (No.  12). 

343.  RiCHEBAND.    Elements  of  Physiology.    Edited  by  J.  Copland,  2nd  Edition,  1829,  p.  167. 

344.  RiEGEL.     Zur  Diagnose  der  Tricuspidainsufficenz.     Berlin.  KHn.  Woch.,  1886,  No.  38, 

p.  621. 

345.  Stokes.    The  Diseases  of  the  Heart  and  Aorta.    Dublin,  1854,  p.  234. 

346.  Walshe.    Diseases  of  the  Heart.    Third  Edition,  p.  376. 

XI.    VENOUS  AND  LIVER  PULSATION 

A  full  bibliography  of  tlus  section  up  to  1893  will  be  found  in  a  paper  I  wrote  on  '  The 
venous  and  liver  pulses  and  the  arrhythmic  contraction  of  the  cardiac  cavities '  in  the 
Journ.  of  Path,  and  BacterioL,  1894,  vol.  ii,  p.  84. 

347.  Babd.     De  Tem-egistrement  graphique  du  pouls  veineux  des  jugulaires  chez  I'homme, 

&c.    Journ.  de  Phys.  et  de  Path,  gen.,  mai  1906. 

348.  Bonniger.    Ueber  den  aiirikularen  Lebervenenpuls.    Charite-Annalen,  xxix.  Jahrgang. 

349.  CuSHNY  AND  Grosh.    The  venous  pulse.    Joui-n.  Amer.  Med.  Assoc,  October  12,  1907. 

350.  Deane.     Respiratory  pulse  curves  and  venous  pulse  in  healthy  people.     Jom-n.  Royal 

Army  Med.  Corps,  June,  1907. 

351.  Deutsch.     Ueber  eine  neue  Methode  zur  Untersuchung  des  Venenpulses.     Congress  f. 

innere  Medizin,  1904. 

352.  DoTOiA.    De  Analyse  van  het  Phlebogram.    Groningen,  1906. 

353.  Fredebicq.     La  seconde  ondulation  positive  (premiere  ondulation  systolique)  du  pouls 

veineux  physiologique  chez  le  chien.     Archives  Internat.  de  Physiologie,  15  juin 
1907,  pp.  1-25. 

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INDEX 


PAGE 

ABDOMINAL  AORTA 

tracings  of      .  .  .  .        85, 86 

pulse  of,  compared  with  the  liver 
pulse        .....     126 
ABDOMINAL  VEINS 

stasis  in       .  .  .  .  .62 

ACCELERATOR  NERVES,     ^ee  Nerves. 
A-C  INTERVAL 

cases  showing  great  increase  of 

337, 361, 364 

definition  of    .         .         .     xviii,  161,  176 

increased         ....      177,  179 

in  cases  of  extra-systole  .         .     160 

significance  of  .         .         .160 

variations  in  duration  of  .     160 

ADAMS-STOKES  SYNDROME  .         .       24 

in  nodal  bradycardia        .     343,  344,  345 

See  also  Heart-Block. 
ADHERENT  PERICARDITOI    . 

liver  pulse  in  ... 

inverted  cardiogram  in 

ADRENALIN       .... 
AFFERENT  NERVES 

See  Nerves  of  the  Heart. 

AGUE 

the  heart  in    . 

AIR,  BELCHING  OF 

after  an  attack  of  angina  pectoris 

AIR  HUNGER    . 

AIR  SUCTION    . 

in  angina  pectoris  . 

ALBUMINURIA 

in  dilatation  of  the  heart 

ALCOHOLIC  HEART 

dilatation  of   . 

rate  in    . 
AMYL  NITRITE 

action  of        .         .         . 
in  angina  pectoris  . 

ANACROTIC  PULSE 

in  aortic  stenosis     . 

ANATOMY  OF  THE  HEART 

ANEURYSM 

cardio-sclerosis  with 
mode  of  death  in  . 
pain  in  ... 


253 
125 

87 
276 


216 

.       50 

26 

59 
50,60 

.     211 

207 
132 

276 
303 

240 
16 

251 
252 

252 


ANGINA  PECTORIS 

air  suction  in  ....       60 

amyl  nitrite  in  ...  .  303 
aortic  aneurysm  with  ...  42 
aortic  regurgitation  with  .  .  242 
aortic  stenosis  with  .  .  .  240 
aortic  valvular  disease  with  .  .  42 
arterial  pressm-e  in  ...       42 

arterial  pressure  during  attacks  of  49,  303 
atheroma  of  coronary  arteries  \nih  42 
belching  of  air  during  an  attack  of  50 
bodily  exertion  causing  .  .  42,  46 
cardio-sclerosis  with.  .  .  42,  304 
case  of  death  due  to  .  .  .50 
cessation    of,    with    dilatation    of 

heart 47 

cessation  of,  with  onset  of  mitral 

regurgitation       ....       47 
character  of  the  attacks  .         .       47 

cold  air  causing       .         .         .  42, 47 

conditions  inducing  an  attack  of  42,  47 
conditions  predisposing  to  an  attack 

of 42,45 

conductivity  in  cases  of  .  .  .43 
constriction  ot  chest  in  .  .  47,  48 
dilatation  absent  in  severe  .  .  202 
disease    of    the    coronary   arteries 

with  ....  46,304,305 
danger  in  slight  attacks  of  .  .50 
death  during  an  attack  of  .  .  48 
definition  of  term  . 
duration  of  the  attacks  of 
effect  of  dilatation  in 
excitability  in  cases  of  . 
excitement  causing 
exhaustion  of  contractility  causing 
exhausted   heart   muscle   and   ex 

hausted  nervous  system  with 
exhaustion  of  left  ventricle  causing 
extra-systoles  dmdng  an  attack  of 

50,  306,  307 
herpes  zoster  compared  with  .       57 

hyperalgesia  after  an  attack  of  50,  51 
hyperalgesic  areas  in  .  .  .40 
impaired  nourishment  of  the  heart 

muscle  causing    .... 
increase  of  urine  in  atack  of    . 
in  mediastino-pericarditis 
mental  excitement  causing 
micturition  after  an  attack  of 
mitral  regurgitation  prevents 


57 
47 
206 
43 
42 
43,193 

57 
46 


42 
24 
253 
47 
50 
47 


396 


INDEX 


PAGE 

ANGINA  PECTORIS  (continued)— 

in  mitral  stenosis  .  .  .  230, 234 
over-exertion  causing  .  .  .  103 
pain  in,  a  viscero-sensory  reflex  .  40 
persistence  of  pain  after  an  attack 

of 50 

pathology  of  heart  vnth        304,  305,  353 
increased  peripheral  resistance  caus- 
ing     ......       43 

perspiration  during  an  attack  of  .  48 
position  assumed  during  an  attack 

of 48 

prognosis  in  .  .  .  .  .50 
pulsus  alternans  with  43,  50, 196,  303,  308 
the  pulse  in  (illustrative  cases)  302-308 
iiTitable  focus  in  spinal  cord  causing 

i-ecuiTcnce  of  .  .  .  .45 
a  reflex  protective  phenomenon  .  45 
region  of  pain  in  ...       40 

resemblance    of,    to    intermittent 

claudication  ....  46 
saliva  increased  in  ...       42 

sense  of  impending  death  during 

an  attack  of  .  .  .  .49 
a  sign  of  impaired  contractility  .  43 
site  of  pain  during  an  attack  of  .  48 
sleeplessness  causing  .  .  250, 270 
state  of  arteries  during  an  attack 

of 49,302 

state  of  heart  during  an  attack  of  .  49 
stimulus-production  with  .  .  43 
symptoms  after  an  attack  of  .       50 

symptoms  during  an  attack  of         .       48 
a    symptom    of    exhausted    con- 
tractility       .         .         .         .43,  193 
a    symptom    of    exhausted    heart 

muscle  .....  42 
suction  of  air  during  an  attack  of  .  50 
summation  of  stimuli  causing  .       43 

tendency  to  recurrent  attacks  of  .  50 
tonicity  with  ....       43 

treatment  by  ammonium  bromide  270 
treatment  by  chloral  .  .  .  270 
treatment  during  an  attack  of  .  53 
treatment  of  condition  inducing  52,  270 
unconsciousness  during  ...  48 
valvular  disease  with  ...  57 
vasomotor  ....  .49, 62 
viscero-motor  reflex  in    .         .         .41 


ANIMALS 

insensitiveness  of  viscera  in 

ANTIARIN 

action  on  tonicity  . 

ANTIFEBRIN     . 


34 

9 
270 


AORTIC  REGURGITATION 
angina  pectoris  in  . 
arteries  visible  in    . 
capillary  pulsation  in 
murmur  characteristic  of 
in  endocarditis 
pulse  in  ... 

facial  aspect  in 
movement  of  liver  in 


PAGE 

240 
242 
92 
241 
240 
219 
241 
242 
241 


AORTA 

in  the  fixation  of  the  heart  .  .  16 
tracings  of  abdominal  .  .  .85,  86 
aneurysm  of,  with  angina  pectoris  .       42 


symptoms  of  heart  failure  due  to    .     242 

AORTIC  STENOSIS  .  .  .  .239 
angina  pectoris  witli  .  .  .  240 
mm-mur  characteristic  of  .  .  239 
pulse  in  .....     239 

AORTIC  VALVE  DISEASE  .  .  238 
angina  pectoris  in  .  .  .  .42 
congenital  .....  239 
liypertrophy  of  the  left  ventricle  in  239 
nose  bleeding  in  .  .  .  .23 
and  pregnancy  ....  260 
after  rheumatism  ....  239 
from  sclerotic  changes     .         .         .     239 

AORTIC  VALVES 

rupture  of 239 

APERIENTS 274 

APEX  BEAT 

in  aortic  regurgitation  .  .  .  241 
auricular  wave  in  .  .  81,86,183,339 
definition  of  .  .  .  .  .77 
due  to  extra-systoles  .  .  .  154 
in  heart-block  ....  183 
how  to  record  .         .         .         .71 

in  nodal  rhythm  .  .  81,321,339 
period  of  contraction  ...  78 
period  of  filling  ....  81 
period  of  relaxation  ...  80 
and  the  retraction  of  the  lung  .       88 

due  to  right  ventricle      .         .  85,  88 

interpretation  of  a  tracing  of  .  .  78 
showing  coupled  beats  .  .  284, 285 
systolic  plateau  in  tracings  of  78,  80,  82 
time  of  opening  of  a.-v.  valves       80,  110 

APEX  OF  HEART 

arrangement  of  muscle- fibres  at 
movement  of . 


17 
17 

31 

20 


APOPLEXY 

pulmonary      ..... 

APPEARANCE  OF  THE  PATIENT 

ARM 

pain  in,  during  an  attack  of  angina 
pectoris       ..... 
development  of       . 
nerve-supply  of       ...         . 
reason  for  heart  pain  felt  in    . 

ARTERIAL  DEGENERATION 

and  high  blood-pressure  .         .     101 

and  cardio-sclerosis        .        243, 245, 247 


48 
39 
39 
40 


INDEX 


397 


ARTERIAL  DEGENERATION  {con- 
tiniied) — 
definition  of    . 
and  extra-systoles 
and  heart  failure     . 
and  the  nodal  rliythm     . 
and  obliteration  of  the  capillaries 
recognition  of  ... 

superficial  arteries  in 


XVUl 

103 
103 
104 
244 
93 
93 


ARTERIAL  PRESSURE 

in  angina  pectoris  .  .  .  .42 
during  attacks  of  angina  pectoris  49,  303 
in  cardiac  asthma  ....  29 
effect  of  capillary  obliteration  on  .  245 
cause  of  .....  98 
in  Cheyne-Stokes  respiration  29,  30,  189 
wath  exhaustion  of  contractility  .  193 
difficulties  in  obtaining  ...  98 
digital  examination  of  .  .  .  93 
effect  of  digitalis  on  .  .  289,369 
diminished  .....  104 
effect  of  dilatation  of  the  heart  on  49,  206 
graphic  records  of  .  .  .  .  100 
heart  failure  with  increased  .  .  102 
causes  of  increased  .  .  .  101 
method  of  measuring  ...  98 
increased  by  diminution  of  capil- 
lary field     102 

action  of  nitrites  on  .  .  .276 
with  the  pulsus  alternans  .  196,  303 
resistance     of     arterial     walls     in 

estimating  .....     100 
significance  of  a  fall  of    .         .         .     104 

y»— treatment  of  high  .         .         .         .103 
in  valvular  disease  .         .         .     103 

ARTERIAL  PULSE 

natiu-e  of  movements  of .         .         .91 

ARTERIAL  WALLS 

condition  of  .  .  .  .  .93 
in  estimating  arterial  pressure         .     100 

ARTERIES 

digital  examination  of  .  .  .93 
function  of  elastic  coats  of  .  .  1 
hypertrophy  of  muscular  coat  of  .  245 
inspection  of  .  .  .  .  .92 
in  surgical  operations  how  recog- 
nized .....  91 
state  of,  during  an  attack  of  angina 

pectoris       .         .         .         49,302-308 
visible  movements  of      .         .         .92 

ARTERIOLES 

dilatation     of,     in     exophthalmic 

goitre  .....     133 

dilatation  of,  in  aortic  regurgitation    240 

ARTERIO-SCLEROSIS 

causation  of    .         .         .         .         -     243 

ARTERY  92 

nature  of  movements  of  tortuous  91,  92 
size  of  the      ,         ....       93 


PAGE 

ARTERY  {continued)— 

supplying  a. -v.    bundle,   condition 

of  in  nodal  rhythm  .  .  .  168 
changes  in  radial  due  to  fever  .     216 

ARTIFICIAL  WAVES 

in  tracings      .         .         .         .         .     ."U 1 

ASTHMA,  CARDIAC 

arterial  pressure  with  ...  29 
associated  sj'mptoms  .  .  .28 
in  cardio-sclerosis  ....  246 
conditions  giving  rise  to  .         .       29 

pulse  in  .....       29 

sleep  with  .....  28 
signs  of  .....       28 

treatment  of  .         .         .         .         .     270 

ATHEROMA  OF  CORONARY  ARTERIES 
angina  pectoris  in  .         .         .         .42 

ATROPHY  OF  AURICULAR  MUSCLE  118 

AUDITORY  NERVE 

stimulation  of         .         .         .         .35 

AURICLE 

electro- cardiogram  of  .  .  .  373 
hypertrophy  of  right,  in  tricuspid 

stenosis       .....     238 
starting-place  of  the  heart's  con- 
traction      .....     140 

AURICULAR  DEPRESSION 

in  a  jugular  pulse    ....     109 

AURICULAR  DIASTOLE 

effect  of,  on  the  jugular  pulse  .     109 

AURICULAR  EXTRA-SYSTOLES     .     154 

AURICULAR  HYPERTROPHY 

with     ventricular     jugular     pulse, 
significance  of     .         .         .         .118 

AURICULAR  LIVER  PULSE    .         .     123 
cases  of  .        .         .         .         .      314, 347 

AURICULAR  MOVEMENTS      .         .       77 

AURICULAR  JilUSCLE 

atrophy  of      .         .         .         .         .118 

AURICULAR  PARALYSIS 

evidence  of  .  .  .  .  .118 
and  the  nodal  rhythm     .         .         .     168 

AURICULAR  PAROXYSMAL  TACHY- 
CARDIA     334 

AURICULAR  PRESSURE  CURVE  .     108 

AURICULAR  SYSTOLE 

disappearance   from   normal   place 

in  cardiac  cycle  .  .  117,166,309 
effect  of,  on  radial  pulse  .  .  .184 
murmur  due  to         .         .     177,  232,  365 

AURICULAR  VENOUS  PULSE 

See   JUGULAB  PCLSE. 

AURICULAR  WAVES 

in  apex  tracing,  cause  of  .  .  81,87 
in  apex  tracings,  time  of  .  81,  82,  183 
in  apex  tracings  in  heart-block  183,  339 
in  a  jugular  pulse,  cause  of  .  .  108 
in  the  ventricular  jugular  pulse  118,  326 


398 


INDEX 


PAGE 

AURICULO-VENTRICULAR  BUNDLE 
arterial  supply  of  .  .  .  .14 
in  cardio-sclerosis  .  .  .  184, 248 
relation  of,  to  central  fibrous  body  185 
impaired  in  cases  with  extra- 
systole  ....  151,160 
function  of  fibres  of  .  .  14,  185 
healthy  in  heart-block  .  .  .185 
affected  in  influenza  .  .  .  217 
lesions  of  .  .  .  .  .184 
involved  in  mitral  stenosis 

229,  233,  312,  315,  320,  324 

position  of 13 

isolation  of  .  .  .  .  .13 
condition  of,  in  nodal  rhythm  168,  310 
in  paroxysmal  tachycardia  310,  320,  324 
pathology  of,  illustrative  cases 

310,  312,  315,  320, 324 
in  puerperal  fever  .  .  .  .  217 
in  rheumatic  fever  ....  217 
in  septic  poisoning ....  217 
starting-place  of  heart's  contraction  140 

AURICULO-VENTRICULAR  NODE 

constitution  of  .  .  .  .13 
function  of      .         .         .         .         .14 

position  of 13 

in  cases  of  nodal  rhythm  .         .310 

in  paroxysmal  tachycardia  310,  320,  324 
starting  the  heart's  contraction       .     140 

AUTONOMIC  NERVOUS  SYSTEM 
insensitiveness   of  structures   sup- 
plied by      .         .         .         .         .34 

A.-V.  BUNDLE 

See  Aurictjlo-Ventkicular  Bundle. 

A.-V.  NODE 

See  AuRicuLO- Ventricular  Node. 

A.-V.  SEPTUM 

action  of  muscles  on        .         .         .17 

A.-V.  VALVES 

opening  of      .         .         .         .         .80 


296 
296 


BATHS 

in  treatment  .... 
Nauheim         .... 

BED 

lying  in,  effect  of  on  heart  .     27,  209 

BELLOWS  MURMUR         .         .         .240 
BILIARY  COLIC.     See  Colic. 

BLEEDING 

character  of,  in  capillary  oblitera- 
tion     

in  pregnancy  with  heart  disease 

BLOOD-PRESSURE 

See  Arterial  Pressure. 

BOWEL 

insensitiveness  of    .         .         .         .34 
resection  of,  in  conscious  subject     .       34 


245 
260 


BODILY  COMFORT 

in  treatment  . 
BODILY  EXERTION 

a  cause  of  angina  pectoris 

BRADYCARDIA 

definition  of    . 

loose  employment  of  term 

nodal      .... 

true        .... 

due  to  vagus  stimulation 
BRAIN 

diagram  showing  relation  to  sen- 
sory nerve  ..... 
BRANDY 

during  an  attack  of  angina  pectoris 
BROADBENT'S  SIGN 

in  mediastino-pericarditis 

BROMIDE  OF  AMMONIUM 
in  angina  pectoris  . 
in  exophthalmic  goitre    . 

BROMIDES 

in  cardio-sclerosis   . 

BREASTS 

hyperalgesia  of 

BREATHING 

inability  to  stop 

laboured,    with    dilatation   of    the 

heart 
laboured,  on  exertion     . 
laboiired,  in  heart  failure 
laboured,  a  sign  of  exhaustion  of 

the  heart 
laboured,  with  the  nodal  rhythm 


270 

42,47 

,  138 
56 
.  337 
.  138 
.     139 


36 
53 

254 

66 
270 
134 

251 

56 

27 

27 

28 

27 

28 
28 


exercises  in  oedema  of  the  lungs  210,  213 


rapid,  a  sign  of  pulmonary  stasis 
rapid,  a  sign  of  heart  failure 

BREATHLESSNESS   . 

attacks  of       ...         . 
sudden  attack  of,  in  aortic  regm-gi 

tation  .... 

cause  of  .... 

due  to  infarct  in  lungs    . 
a    symptom    of    exhausted    con 

ti'actility     .... 
treatment  of  . 
■  See  also  Asthma,  Cardiac. 
BRIGHT'S  DISEASE 

mitral  regurgitation  in    . 
pericarditis  in 


27 
27 

26 

28 

242 
26 
32 

193 
270 


236 
220 

274 


CALOMEL   

CAPILLARY  FIELD,  DIMINUTION  OF  46 

a  factor  in  raising  arterial  pressure       102 
etiect  of,  on  the  heart      .         .         .     244 


in  cardio-sclerosis 
effects  of 

effect  of,  on  blood-pressure 
evidences  of    . 


244 
244 
245 
244 


INDEX 


399 


CAPILLARY  PULSATION 

in  aortic  regurgitation 

CARDIAC  ASPIRATION 
due  to  ventricular  systole 
causing  movements  of  the  liver 

CARDIAC  ASTHMA.     See  Asthma. 

CARDIAC  CYCLE 

diagram  of  events  in  a    . 

CARDIAC  NEURASTHENIA     . 

CARDIAC  NEUROSIS 


241,321,324 


82 
82 


108 
56 
56 


CARDIAC  RESPONSE 

in  cardio-sclerosis  ....  246 

limitation  of,  a  sign  of  heart  failure  4 

and  prognosis          ....  266 

CARDIOGRAM 

nature  of  a  .  .  .  .  .18 
inverted  ....  83,84,87 

CARDIO-MOTOR  CENTRES      .         .       15 

CARDIO-SCLEROSIS 

and  aneui-ysm  ....  251 
and  angina  pectoris  .  .  42,  304 
and  arterial  degeneration  .  .  243 
a.-v.  bundle  in  ...  .  184 
blood-pressm-e  in  .  .  .  .  247 
cardiac  asthma  in  .  .  .  28,  246 
change  in  symptoms  with  dilatation  246 
and  chloroform  ....  261 
condition  of  arteries  in  .  .  .  245 
Cheyne-Stokes  respiration  in  .  29,  248 
exhaustion  of  conductivity  in  ,     184 

exhaustion  of  contractility  in  .  .  193 
definition  of    .         .         .         .    xviii,  243 

diet  in 273 

dilatation  of  the  heart  in  .  206,  248 
disease  of  the  kidneys  with  .  .  244 
effect  of  digitalis  in  .  .  .  286 
etiology  .....     243 

extra- systQles  in  .  .  .  .  246 
extreme,  without  dilatation  ,  .  202 
heart-block  due  to  .  .  .184,  246 
illustrative  cases  .  .•  .  351, 354 
irregularities  in  .  .  .  246, 352 
mitral  regurgitation  in  .  .  .  236 
murmurs  in  .  .  .  .  .  247 
nodal  rhythm  in  .  .  142,  168, 247 
with  the  nodal  rhythm,  effect  of 

digitalis  in 172 

paroxysmal  tachycardia  in  247,  324 

pathology  of  .  .  245,328,353,355 
primitive  cardiac  tissue  in       .         .     248 

prognosis  in 248 

progress  of  ....  .  243 
pulsus  alternans  with 

196,  197,  248,  352,  354 
reason  for  variety  of  symptoms  in  .  248 
reserve  force  in  ...  .  247 
of  rheumatic  origin  .         .         .     243 

sensory  phenomena  in    .         .         .58 


248 
245 
245 
244 
249 
41 

216 

107 

91 

75 

113 


270 


CARDIO-SCLEROSIS  {continued)— 
significance  of  cardiac  asthma  in 
symptoms  of 
diversity  of  symptoms  in 
and  syphilis    . 
treatment  of  . 
viscero-motor  reflex  in    . 

CARDITIS 

produced  by  febrile  affections 

CAROTID  ARTERY 

relation  of,  to  jugular  vein 
CAROTID  PULSE 

movement  due  to    . 

as  a  standard  .... 

CAROTID  WAVE 

in  the  jugular  pulse 

CASES  ILLUSTRATING 

effect   of   ammonium    bromide   in 
angina  pectoris   .... 

pathology  of  cardio-sclerosis  338, 353,  355 

chloroform  and  cardio-sclerosis       .     261 

effect  of  digitalis  on  the  heart 

356, 360, 361, 364 

effect  of  fear  on  the  heart        .         .     262 

heart-block      ....     187,  188 

relation  of  heart-block  to  the  nodal 
rhythm 364 

danger  of  heart  disease  and  preg- 
nancy .....     259 

heart's  power  of  recovery        .         .     266 

effects   of   digitalis   on   the   nodal 
rhythm        ....     283,284 

the      inception      of      the 
rhythm 

nodal  bradycardia   . 

the      pathology      of      the 

rhythm  .         .     312,316,320,324 

paroxysmal  tachycardia 

320,  324,  328,  329 

significance  of  the  pulsus  alternans     199 

character  of  pulse  in  angina  pectoris 

302-308 

severe  heart  affection  in  pneumonia    223 

CELLULAR  FOCI 

in  heart  muscle,  in  rheumatic  fever 

CENTRAL  FIBROUS  BODY 

function  of  ....  . 
position  of  ....  . 
relation  of,  to  a.-v.  bundle 

CEREBRAL  ANAEMIA      . 

in  heart-block         .... 

CEREBRAL  EMBOLISM 

in  mitral  stenosis    .... 
CEREBRO-SPINAL  NERVOUS  SYS- 
TEM   

CERVICAL  FASCIA 

in  the  fixation  of  the  heart 

CERVICAL  NERVES.     See  Nerves. 


nodal 
.  309-333 
.  337-349 
nodal 


221 

16 
16 

185 

23 

187 

234 
34 
16 


400 


INDEX 


PAGE 

CHEST,  CONSTRICTION  OF  .  22,  130 
in  angina  pectoris  .  .  .  41, 48 
during  an  attack  of  angina  pectoris  49 
a  viscero-motor  reflex    .         .         .41 

CHEST-WALL 

hyperalgesia  of,  in  dilatation  of  the 
heart 47,203 

CHEYNE-STOKES  RESPIRATION  .       29 

artificial  production  of  .  .  .30 
arterial  pressure  in  .         .       29,  189 

with  Bright' s  disease  ...  30 
in  cardio-sclerosis  .  .  29,  206,  248 
condition  of  heart  in  .  .  .29 
conditions  simulating  ...  30 
consciousness  dui'ing  apnoeic  stage  31 
effect  of  dilatation  of  the  heart  on  .  206 
in  heart-block  ....     189 

hiccough  in  .  .  .  .  .29 
John  Hunter's  description  of  .       31 

mental  condition  in  .  .  .31 
prognosis  in  .  .  .  .  .30 
significance  of,  in  cardio-sclerosis  .  248 
dming  sleep  .....  29 
suffering  due  to  .  .  .  .30 
talking  dm'ing  apnoeic  stage  .  .  31 
treatment  of  .  .  .  .  30, 270 
twitching  of  muscles  in  .         .         .29 

CHILDREN 

periodic  respiration  in  .  .  .30 
heart  uregularity  in        .       140,  142,  146 

CHLORAL 270 

in  angina  pectoris  ....  54 
in  cardio-sclerosis  ....     251 

CHLOROFORM 

in  cardio-sclerosis  ....  261 

fitness  of  tlie  patient  to  take  .         .  262 

and  heart  affections        .         .         .  261 

and  heart-block  ....  263 
and  imperfect  oxygenation  of  the 

blood.         .         .  .         .  261 

and  irregular  heart-action       .         .  263 

and  pregnancy        ....  260 

and  the  status  lymphaticus     .         .  262 

and  valvular  disease        .         .         .  261 

CICATRIZATION 

after  rheumatic  fever      .         .         .     222 

CIRCULATION 

object  of  the  .....         1 

CLASSIFICATION  OF  SYAEPTOMS 

in  visceral  disease  ....       33 

CLINICAL  EVIDENCE 

of  the  nodal  rhythm        .         .         .     309 

COLD 

effect  of,  on  the  heart's  rate    .         .     139 

COLD  AIR 

exposure    to,    a    cause    of    angina 
pectoris        ....         42, 47 


PAGE 

COLD  BATHS 

in  exophthalmic  goitre   .         .         .134 

COLD  HANDS 

in  the  X  disease      ....       60 

COLIC,  BILIARY 

hyperalgesia  in       .         ,         .         .37 
situation  of  pain  in  ...       38 

COLIC,  RENAL 

situation  of  pain  in  ...       39 

COMPARISON  OF  AURICULAR  PRES- 
SURE 

with  the  jugular  pulse     .         .         .     107 

COMPENSATORY  PAUSE 
cause  of  ... 


COMPLAINTS,  CHIEF 

COMPRESSION  OF  CHEST 

sense  of  . 


xviii,  162 
.       21 

22, 130 

CONDUCTIVITY         ....         8 

aftections  of 175 

and  angina  pectoris  ...  43 
cause  of  depressed  .         .         .185 

depression  of,  in  febrile  affections 

of  the  heart  .  .  .  .217 
depressed  in  rheumatic  hearts  .  184 
depressed  in  cardio-sclerosis  .  .  184 
depression  of,  increased  by  digitalis 

186,  288,  361, 362 
method  of  recognizing  depression  of  175 
significance  of  depression  of  .  .186 
prognosis  in  depression  of  .  .  189 
influence  of  rest  upon  .  .  .  177 
irregularity  due  to  depression  of  142,  179 
manner  in  which  depression  of  is 

produced  in  mitral  stenosis         .     229 

CONGENITAL  AFFECTIONS  OF  THE 
HEART 

etiology  .....     256 

prognosis  .....  257 
symptoms  .....  256 
treatment       .....     257 

CONGENITAL  DEFECTS  OF  AORTIC 
VALVES 239 

CONSCIOUSNESS 

loss  of 23 

dvu-ing   apnoeic   stage   of   Cheyne- 
Stokes  respiration       ...       31 

CONSCIOUS  SUBJECT 

resection  of  bowel  in       .         .         .34 

CONSTIPATION 

in  heart  failure        ....     274 

CONSTRICTION  OF  CHEST.     See  Chest. 

CONTRACTILITY       ...  8,  191 

angina  pectoris  due  to  exhaustion 
of 43,  193 


INDEX 


401 


PAGE 

CONTRACTILITY  {continued)— 

arterial  pressure  with  exhaustion  of  193 
effect  of  digitaHs  on  .  .  .  287 
conditions  inducing  exhaustion  of  .  192 
exhaustion  of,  due  to  degeneration 

of  muscle  .  .  .  .  .192 
exhaustion  of,  due  to  dilatation  ,  192 
exhaustion    of,    due    to    imperfect 

nutrition  .....  192 
exhaustion  of,  due  to  increased  rate  192 
exhaustion  of,  due  to  obstruction  to 

the  heart's  work  .         .         .     192 

effect  of  rest  on  exhausted  .  .  199 
exhaustion  of,  in  pneumonia  .  .  218 
exhaustion  of,  the  cause  of  angina 

pectoris  .....  43 
necessity   for  recognizing  exliaus- 

tionof 190 

prognosis  of  exhaustion  of  .  .  198 
pulsus    alternans,    a    symptom    of 

exhaustion  of  .  .  .  .194 
reserve  force  of  .  .  .  .192 
reflex  symptoms  of  exhaustion  of  .  193 
symptoms    of    exhaustion    of,    in 

rheumatic  hearts  .         .         .     193 

symptoms    of    exliaustion    of,    in 

cardio-sclerosis  .  .  .  .193 
symptoms  of  exhaustion  of     .         .     192 

CONVALESCENCE 

after  febrile  affections  of  the  heart     227 


COR  BOVINUM  . 


239 


CORRIGAN'S  PULSE 


CORONARY  ARTERIES 

in  cases  of  angina  pectoris 

42,  46,  304,  305 

heart-block  in  sclerosis  of        .         .     185 

CORONARY  SINUS 

heart's  contraction  starting  at         .        13 
how  regurgitation  into  is  prevented       16 


240 


COUPLED  BEATS 

due  to  digitalis,  significance  of 

283,  284, 288 
of  the  nodal  rhythm  distinct  from 
extra-systoles      ....     286 

CYANOSIS 

in  congenital  heart  affections  .         .     256 
oxygen  in        ....         .     279 


DEATH 

dm-ing  an  attack  of  angina  pectoris      48 

due  to  digitalis        .         .         .  186,291 

due  to  heart-block           .         .  .189 

sense    of    impending,    during  an 

attack  of  angina  pectoris     .  .       49 

sense    of    impending,    during  an 

attack  of  palpitation  .         .  .135 


PAGE 

DEFINITIONS 

apex  beat 77 

a-c  interval  ....  xviii,  176 
auricular  venous  pulse  .  .  .  xviii 
auriculo-ventricular  node  .  .  xviii 
auriculo-ventricular  bundle  .  .  xviii 
cardiac  asthma  ....  28 
cardio-sclerosis        ....  xviii 

carditis 216 

conductivity  ....    xviii,  175 

contractility xviii 

extra-systole xviii 

heart-block  ....  xix,  175 
hyperalgesia  .....  xix 
myogenic  theory  ....  xix 
nodal  rliythm  .         .         .      xix,  .309 

palpitation      ....  xix 

paroxysmal  tachycardia  .      xix,  172 

primitive  cardiac  tissue  .  .  .  xix 
pulsus  alternans  ....  xix 
pulsus  bigeminus  ....  xix 
sino-auricular  node  .         .         .     xix 

sphygmogram  ....  95 
tonicity  .....     xix 

ventricular  rhythm  .         .         .     175 

ventricular  venous  pulse  .         .      xx 

viscero- motor  reflex  .  .  .  xx 
viscero-sensory  reflex      .         .         .      xx 

DEGENERATION  OF  HEART  MUSCLE 

See  Cardio-Sclerosis. 

DELUSIONS 25 

DEPRESSOR  NERVE 

See  Nerves  of  the  Heart. 

DESIRE  TO  BREATHE  ...   26 

DEVELOPMENT 

of  arms  .....  39 
of  the  heart 11 

DIABETES 

pericarditis  in         ....     220 

DIAGNOSES 

mistaken,  how  they  arise         .         .215 

DIAGRAM 

showing  relation  of  brain,  spinal 
cord  and  skin  to  a  sensory  nerve       36 

DIAPHRAGM 

in  the  fixation  of  the  heart      .         .       16 

DIASTOLIC  MITRAL  MURMUR 

^ee  Murmurs. 

DIASTOLIC  NOTCH 

in  a  sphygmogram  ...       96 

DIASTOLIC  PERIOD 

in  a  sphygmogram  ...       95 

DIASTOLIC  WAVE 

in  the  jugular  pulse         .         .         .     113 


MACKENZIE 


D  d 


402 


INDEX 


DICROTIC  WAVE 

cause  of 

DIET 

in  cardio-sclerosis 
in  treatment  . 


PAGE 

96 

273 
271 


DIGESTIVE  TUBE 

nature  of  symptoms  produced  by  ,       34 

DIGITAL  EXAMINATION 

of  the  arteries         ....  93 

of  the  arterial  pressure    ...  93 

of  the  arterial  pulse         ...  90 

DIGITALIS 

and  blood-pressme  .  .  289, 369 
in  cardio-sclerosis  ....  251 
causing  heart-block  .  287,  360,  365 
causing  intermittent  pulse  .  .186 
causing  pulsus  alternans  .      197,  288 

conditions  in  which  it  is  useful  .  290 
conditions  in  which  it  is  useless  .  291 
effect  on  conductivity  .  .  287, 365 
increasing  depression  of  conduc- 
tivity .  .  .  186,360,365 
effect  on  contractility  .  .  .  288 
effect  on  dilatation  of  the  heart  .  282 
action  of  different  preparations  .  281 
effect  on  dropsy  ....  208 
effect  on  enlargement  of  the  liver  .  286 
action  of,  on  the  human  heart  281,  356 
illustrative  cases,  showing  effects  of 

356,  360,  361,  364 

effect  on  the  nodal  rhythm      .     172,  282 

susceptibility  of  nodal  rhythm  to  .     286 

effect    on    nodal    rhythm    due    to 

cardio-sclerosis    ....     287 

in  practice 290 

use  of,  in  prognosis  .  .  .211 
effect  on  rate  .....  282 
reason  for  uncertain  action  of  .  281 
reason  for  contradictory  effects  of  .  286 
significance  of  coupled  beats  pro- 
duced by 285 

and  slow  respiration  .  .  .31 
sudden  death  due  to  .  .  186,291 
action  on  tonicity  ...  9,  282 

in  the  treatment  of  dilatation  .     211 

DIGITALIS,  SQUILL  AND  CALOMEL 
in  cardiac  dropsy    .         .         .         .212 

DILATATION  OF  THE  HEART 

in  febrile  affections  .         .         ,     219 

albuminuria  in        .         .         .         .211 

alcoholic 207 

effect  on  angina  pectoris  .         .     206 

effect  on  arterial  pressure        .         .     206 
laboured  breathing  in    ' .         .         .       27 
effect  on  cardiac  asthma  .         .     206 

in  cardio-sclerosis  .         .         .      206, 248 
cause  of .         .         .         .         .         .     201 

effect  on  Cheyne-Stokes  respiration    206 


DILATATION  OF  THE  HEART  (con- 
♦         tinned) — 

consequences  of      . 
exhaustion  of  contractility  due  to 
effect  of  digitalis  on        .         .         . 
displacement  of  lung  due  to    . 
causing  epigastric  pulsation 
due  to  fever    ..... 
effect  of,  on  the  jugular  pulse 
enlarged  liver  in      . 
manner  of  production  of 
manner   in  which    symptoms   ai'e 
produced    .         .         .         .         . 
and  mitral  regurgitation 
and  mitral  stenosis 
with  the  nodal  rhythm   . 
its  significance  in  the  nodal  rhythm 
oedema  of  the  lungs  in    . 
in  paroxysmal  tachycardia 
significance     of,     in     paroxysmal 
tachycardia         .         .         .         . 
the  position  of  the  heart  in 
and  pregnancy        .... 
prognosis  in    . 

I'eflex  symptoms  produced  bj' 
in  rheumatic  fever 
signs  of  . 

bearing  of,  on  treatment 
urinary  symptoms  in 


205 
192 

282 
206 
83,84 
215 
205 
208 
203 

205 
235 
233 
170 
171 
208 
207 

172 
.  204 
.  258 
.  211 
.  203 
.  222 
.  203 
207,211 
.  210 

DILATATION  OF  LEFT  VENTRICLE 
in  mitral  stenosis     .         .         .     203,  229 

DIPHTHERIA 

the  condition  of  the  heart  in         214,  224 
fatal  syncope  in      .         .         .         .     225 

DIPLOCOCCUS  RHEUMATICUS       .     221 

DISAPPEARANCE  OF  PRESYSTOLIC 
MURMUR 223 

DISEASE,  NATURE  OF 

shown  by  irregularities   .         .         .     217 

DISPLACEMENT  OF  THE  CHAMBERS 
OF  THE  HEART 
in  dilatation 203 

DISSOCIATION  OF  PLACES 

in  starting  the  heart's  contraction       13 

DIURESIS  IN  HEART  FAILURE 

cause  of  profuse      ....     212 

DIURETIN 212 

DIZZINESS 23 

DOG 

irregular  heart-action  in  .         .     144 

DORSAL  NERVES 

peculiar  field  supplied  by  upper      .       40 

DROPSY 

in  arms  and  face     ....     207 
effect  of  digitalis  in  .         .         .     208 


INDEX 


403 


DROPSY  (continued)— 

dilatation  of  the  heart  causing 
a  sign  of  dilatation  of  the  heart 
manner  of  onset  of 
in  cases  of  nodal  rhythm  .      1 

in  paroxysmal  tachycardia     .      1 
in  rheumatic  heart  cases 
the  secretion  of  urine  witli 
significance  of 
treatment  of  . 

DRUGS 

in  treatment 

DYSPNOEA.     See  Breathlessxess. 


47,  200 
.  206 
.  206 
70, 208 
73,  207 
.  207 
.  207 
.  207 
.  211 

.     275 


OF      REFLEX 


E 


meaning  of  period 


ELECTRO-CARDIOGRAM 

of  the  auricle  . 
of  the  ventricle 
the  normal 
of  heart-block 
of  the  nodal  rhythm 
of  extra-systoles 


75, 112 

.  370 

.  373 

.  373 

.  372 

.  373 

.  374 

.  375 


ELECTRIC  CHANGES 
due  to  heart  beat    . 
in  muscular  tissue  . 

.     370 
.     370 

EMBRYOCARDIA 

loose  employment  of  term 

.       56 

ENDOCARDITIS 
in  acute  fevers 
malignant 
misleading  term 
symptoms  of  . 

.     214 
.     221 
.     215 

219,  "226 

ENEMATA 

.     274 

ENLARGEMENT  OF  THE  LIVER  .     122 

EPIGASTRIC  PULSATION 

causes  of         .         .         . 
in  fevers 

83,85 
.     216 

in  pernicious  anaemia     . 

in  typhoid  fever 

and     the     shock     of     ventr 

systole 
time  of  . 

.       85 
.       84 
icular 

.       89 
.       84 

EPILEPTIC  ATTACKS       . 
due  to  heart-block 

24,  342 

.     187 

ERECTOR-SPINAE  MUSCLES 

tenderness  of,  in  liver  enlargement     123 

ERYSIPELAS 

a  cause  of  mitral  stenosis         .         .     229 
the  heart  in    .         .         .         .         .     214 


FACTOR    IN    HEART 


ESSENTIAL 
FAILURE 

ESSENTIAL  PRINCIPLE  IN  TREAT- 
MENT        


2,268 


268 


EXAGGERATION 
SYMPTOMS 

in  nervous  people   .... 

EXCITABILITY  OF  THE  HEART  . 

and  angina  pectoris 

EXCITEMENT 

a  cause  of  angina  pectoris 

EXERCISES 

rules  for  employment  of 

special    ...... 

value  of  different  forms  of 
breatliing        ..... 

EXHAUSTED  HEART  MUSCLE 
the  cause  of  angina  pectoris    . 

EXHAUSTING  DISEASES 
heart-rate  increased  in    . 

EXHAUSTION 

sense  of  . 

EXOPHTHALMIC  GOITRE 
arteries  visible  in    . 
peripheral  circulation  in 
treatment  of  . 

EXPECTORATION 

blood-stained,  in  dilatation  of  the 
heart  ...... 


PAGE 


EXPERIMENTAL    EVIDENCE 
THE  NODAL  RHYTHM 


OF 


EXPERIMENTAL      STIMULATION 
OF  VAGUS  NERVE 


55 

8 
43 

42 

293 
295 
294 
213 

42 

132 

OO 


92 
133 
134 


206 


120 


145 


EXTRA-SYSTOLES 

electro-cardiogram  of  .  .  .  375 
extra-systoles,  definition  of  .  xviii,  148 
extra-systoles,  classification  of  .  151 
extra-systoles,  in  angina  pectoris 

50,  306,  307 
extra-systoles  and  variations  of  the 

a-c interval         ....     161 
extra-systoles  in  acute  affections     .     218 
extra-systoles  in  arterial  degenera- 
tion     103 

extra-systoles,  am'icular  .         .154 

extra-systoles  and  the  a.-v.  bundle  160 
extra-systoles  distinct  from  coupled 

beats  of  nodal  rhythm  .  .  286 
extra-systole  evidence  of  impair- 
ment of  a.-v.  bundle  .  .  .  151 
extra-systole  with  cardiac  asthma  29 
extra-systole  with  cardio-sclerosis  .  248 
extra-systole  cause  of  compensa- 
tory pause  .....  161 
extra-systole,     character     of     the 

irregularity  .         .         .         .148 

extra-systoles,  conditions  inducing     163 


extra-systole  due  to  digitalis 
extra-systoles,  etiology 


359,  368 
150, 163 


D  d  2 


404 


INDEX 


lEXTRA-SYSTOLES  (continued)— 

extra-systole,  relationship  to  heart- 
block           185 

extra-systole,  nodal         .         .         .  157 

extra-systole,  effect  on  mind            .  55 

extra-systoles  and  the  nodal  rhythm  164 

place  of  origin  of  ventricular            .  151 
extra-systoles  and  the  primitive  car- 
diac tube    .         .         .         .         .162 

extra-systole  prognosis  of        .         .  164 

extra-systoles  and  pulsus  alternans  195 
extra-systoles    distinct    from    the 

pulsus  alternans  .         .         .198 

extra-systoles,  sensations  produced 

by 164 

extra-systoles,  sounds  due  to  .  150 
extra-systoles,  treatment  of  65,  164,  250 
extra-systole,  ventricular  inter- 
polated .....  151 
extra-systoles,  varieties  of  .  .  141 
extra-systoles  in  the  X  disease        .  62 

FACIAL  ASPECT  ....  20 
in  aortic  regm-gitation  .  .  .  242 
during  an  attack  of  angina  pectoris       48 

FAINTING 23 

FATTY  DEGENERATION  OF  THE 
HEART 243,245 

in  acute  febrile  affection  .         .     216 

pulsus  alternans  in  .         .         .196 

FEBRILE  AFFECTIONS  OF  THE 
HEART 

convalescence  after 
symptoms  in  . 
treatment  of  . 
a.-v.  bundle  affected  in  . 


FEVER 

dilatation  of  the  heart  in 
effect  of,  on  the  heart 
heart  symptoms  in 
pulse-rate  in  . 
varying  reaction  on  heart  of   . 

FINGERS 

clubbing  of     . 

FIXATION  OF  THE  HEART   . 

FOCUS,       IRRITABLE,      IN      THE 
SPINAL  CORD        .... 
due  to  angina  pectoris    . 
a  cause  of  the  tendency  to  recurrent 

attacks  of  angina  pectoris   . 
symptoms  of  . 

FRACTURED  TIBIA 

pulmonary  infarct  from 

FUNCTIONS      OF      THE      HEART 
MUSCLE-FIBRES    ....         7 

FUNCTIONS   OF  THE   PRIMITIVE 
CARDIAC  TUBE      .         .         .       11,141 


227 
216 
226 
217 

219 
214 
215 
215 
216 

256 
203 

37 
45 

50 
37 

32 


GANGLION  CELLS    ....       14 
their  function  ....       19 

GALVANOMETER   .    .    .    .371 

GANGRENE  OF  LEG 

after  intermittent  claudication        .       46 

GASKELL'S  BRIDGE,    ^ee  Auriculo- 
Ventricular  Bundle. 

GASTRIC  ULCER.     See  Ulcer. 

GIDDINESS 23 

GRAPHIC  RECORDS 

of  arterial  pressure  .  .  .'100 
of  heart  movements  ...  77 
of  the  jugular  pulse  .  .  .  106 
use  of 67 

GRAVE  CONDITIONS 

due  to  the  nodal  rhythm         .         .     170 

GRIPPING  OF  CHEST 

in  angina  pectoris  .         .         .         .41 


HALLUCINATIONS    ....       25 

HAEMOPTYSIS 

in  mitral  stenosis    ....     234 

HAEMORRHAGES      ....       23 

HALLER'S  OBSERVATION 

of  the  insensitiveness  of  the  viscera       35 

HARVEY'S  OBSERVATION 

on  the  insensitiveness  of  the  heart       34 

HEALTHY  PEOPLE 

sinus  irregularity  in         .         .         .     146 

HEART 

acute  febrile  affections  of  the 

in  ague  ...... 

in  an  attack  of  angina  pectoris 
apex,  arrangement  of  muscle  fibres 

at        .....         . 

a.-v.  bundle  in  rheumatic  affections 

of 

a.-v.  bundle  in  acute  affections  of  . 


4,216 

,  216 

49 

17 

184 
184 

HEART  ABNORMALITIES 

mental  state  induced  by  .         .       56 

HEART'S  ACTION  WITH  THE  NODAL 
RHYTHM.     See  Nodal  Rhythm. 

HEART-BLOCK 24 

in  acute  affections  .         .         .     185 

apex  beat  in  .  .  .  .  .  183 
auricular  waves  in  apex  tracings  in 

cases  of  .  .  .  .  .81 
a.-v.  bundle  healthy  in  .  .  .  185 
due  to  cardio-sclerosis  .  .  .  247 
produced  by  swallowing  .         .     365 

cases  illustrating  relation  of,  to  the 

nodal  rhythm      .         .         .      337,364 


INDEX 


405 


HEART-BLOCK   (continued)— 

Cheyne-Stokes  respiration  in 

189 

and  chloroform 

263 

definition  of  . 

xix 

175 

due  to  digitalis 

186 

287 

cases  of,  produced  by  digitalis 

360 

361 

electro-cardiogram  of 

373 

and  epileptiform  attacks 

187 

etiology 

184 

relationship  to  extra-systole 

185 

inexcitability  of  ventricle  in 

189 

relationship  to  nodal  rliythm 

185 

prognosis  in    . 

189 

due  to  septic  poisoning   . 

218 

symptoms  in  a  case  of     . 

187 

symptoms  associated  with 

187 

and  syncopal  attacks 

187 

producing  slow  pulse-rate 

.      138 

142 

vagus  stimulation  producing 

186 

treatment  of  . 

190 

HEART  CHANGES 

with  increased  rate  .         .         .135 

HEART,  CONDITION  OF 

in  Cheyne-Stokes  respiration  .         .       29 

HEART,  CONGENITAL  AFFECTION 
OF 256 

HEART'S  CONTRACTION 

electrical  changes  due  to  .         .     370 

normal  starting-point  of  .         12,  15 

starting  in  the  primitive  cardiac 


tube 

starting-places  of    . 
starting  in  the  auricle 
starting  in  the  a. -v.  bundle 
starting  in  the  a.  -v.  node 
starting  in  the  sinus-venosus 


11, 


141 
141 
141 
141 
141 
141 


HEART,  DEVELOPMENT  OF  THE  .       11 


HEART  DILATATION 

in  acute  febrile  affections  .  .  219 
and  blood- pressure  ...       47 

and  cessation  of  angina  pectoris  .  47 
and  dropsy  .....  47 
and  epigastric  pulsation  .         83,  84 

laboured  breathing  in  .  .  .27 
and  mitral  regm'gitation  .         .       47 

HEART  IN  DIPHTHERIA         .     214,  224 

HEART,  EMBARRASSMENT  OF      .         3 
by  pericardial  effusion    .         .         .     220 

HEART  IN  ERYSIPELAS         .        .     214 

HEART  EXHAUSTION 

labom-ed  breathing  in  .  .  .  28 
from  obstruction  to  its  work  .  .251 
from  want  of  exercise  .  .  .  293 
from  want  of  rest    ....       47 


PAGE 

HEART  FAILURE 

and  arterial  degeneration        .  .  103 

with  increased  arterial  pressure  .  102 

constipation  in        ...  .  274 

essential  factor  in   .         .         .  3,  268 

with  a  fractured  leg         .         .  .  209 

jaundice  in     .         .         .         .  .  125 

means  exhaustion  of  reserv'e  force  2,  3 

mitral  stenosis  induces    .         .  .  229 

muscle  exhaustion  in       .         .  .  235 

nature  of  symptoms  in    .         .  .  3 

and  the  nodal  rhythm              .  .168 

cause  of  recovery  from    ...  3 

due  to  valve  defects        .         .  .  228 

w^asting  in       ....  .  209 

HEART,  FEBRILE     .        .         .        .215 

HEART,     FEBRILE     AFFECTIONS 
OF  THE 216 


HEART,  FIXATION  OF    . 


17, 204 


HEART,  FUNCTIONAL  ANATOMY 
OF 16 

HEART  IN  INFLUENZA  .        .        .214 

HEART,     INSENSITIVENESS     OF 
THE 34 

HEART  IRREGULARITY 

classification  .... 

significance  of         .         .         . 

during  attacks  of  angina  pectoris 

due  to  failm-e  of  conduction    . 

due  to  depression  of  conductivity 

consciousness  of      . 

meaning  of  term  '  nodal  rhj'^thm  ' 

in  myocarditis 

significance  of  in  pneumonia  . 

due  to  respii-ation 

during  slow  respiration 

reveals  the  pathology  of  the  heart 

140, 
sensation  produced  by 
arising  at  the  sinus 
arising  at  the  sinus,  character  of 
arising  at  the  sinus,  etiology  of 
arising  at  the  sinus,  prognosis  of 
arising  at  the  sinus,  symptoms  of 
arising  at  the  sinus,  symptoms  asso 

ciated  ^^^th 
arising  at  tlie  sinus,  due  to  vagus 

stimulation 
in  X  disease    .... 


141 
140 

50 
142 
179 

22 
166 
217 
223 
144 

31 

217 
22 
141 
143 
144 
146 
145 

145 

145 
62 


HEART  MOVEMENTS 

graphic  records  of  .         .         .77 

HEART  MUSCLE 

angina  pectoris  in  exhaustion  of      42,  58 
angina  pectoris  in  degeneration  of      42 
characteristics  of  function  of  fibres 
of 9 


406 


INDEX 


HEART  IVrUSCLE  (continued)— 

classification  of  functions  of  fibres  of 
conditions  exhausting  reserve  force 

of 

co-ordination  of  functions  of  . 
development  of       .         .         . 
estimation  of  reserve  force  of 
function*cf  conductivity 
function  of  contractility 
function  of  excitability 
function  of  stimulus  production 
function  of  tonicity 
unequal  endowment  of  functions  of 

fibres  .... 

unequal  exhaustion  of  functions  of 

fibres  .... 

impaired  nourishment  of,  a  cause 

of  angina  pectoris 
importance  of         .         .         • 
involved  in  mitral  stenosis 
reserve  force  of       .         .         . 
sclerotic  changes  in 

HEART,  NATURE   OF  SYAIPTOMS 
PRODUCED  BY      .         .        . 

HEART  OVERSTRAIN      . 

HEART,     PERCEPTIBLE      MOVE 
MENTS  OF       ...         . 


PAGE 


3 

9 

7 
20 


10 

42 
2 

230 
2 

229 

32 
132 


HEART  IN  PNEUMONIA 


76,77 
214,  223 


HEART  IN  RHEUMATIC  FEVER 


HEART,  RUPTURE  OF 


214,  221 
103,  202 


heart;    POSITION    OF,    IN    THE 
CHEST 76 

HEART  IN  PREGNANCY         .         .     258 

See  Pkegnancy. 

HEART- RATE 

in  alcoholics  .         .         .         .132 

cause  of  increased  .  .  .  .136 
effect  of  cold  on  ...  .  139 
continuously  increased  .  .  .  131 
exhaustion  of  contractility  due  to 

increased  .....  192 
difficulties  in  reckoning  increased  .  134 
effect  of  digitalis  on  .  .  .  282 
increased  on  exertion  .  .  .  129 
increased  in  exhausting  diseases  .  132 
in  exophthalmic  goitre  .  .  .133 
increased  frequency  of  .  .  .  128 
meaning  of  increased  .  .  .130 
in  myocardial  affections  .         .     131 

increased  in  neurotic  people    .         .     132 

the  normal 129 

in  palpitation  ....     134 

in  pregnancy 132 

in  tuberculosis  .  .  .  .132 
in  valvular  disease  .         .         .     131 

HEART  REACTION 

to  the  nature  of  the  fever        .         .     214 

HEART,  RELATIONSHIP  TO  SEN- 
SORY NERVES       ....       39 


HEART  IN  SEPTIC  INFECTION  214,  225 

HEART,  THE  SOLDIER'S         .         .     132 

HEART  SOUNDS 

diu'ing  an  attack  of  angina  pec- 
toris     50,270 

uith  alternating  rhythm          .  .     198 

in  depressed  conductivity        .  .     176 

due  to  extra-systoles       .         .  142,  150 

with  pulsus  bigeminus    .         .  .151 

\\ith  sinus  irregularity    .         .  .     145 

HEART,  SPASM  OF,  IMPOSSIBLE  .       44 

HEART'S  STRENGTH 

standard  of  measurement  of   .         .         4 

HEART  IN  TYPHOID  FEVER      209,  214 

HEART,  VENTRICULAR  RHYTHM     182 

HELLEBOREIN  .         .         .         .291 

HEMIPLEGIA 

in  acute  febrile  affections        .         .     219 

HERPES  ZOSTER 

eruption  of,  in  arm  ...       40 

pain  of  simulating  angina  pectoris  .       57 

HIBERNATING  ANIMAL 

and  periodic  respiration  .         .       30 

HICCOUGH    IN    CHEYNE-STOKES 
RESPIRATION        ....      29 

HIS'  BUNDLE.  See  Aueiculo-Ventki- 
CULAR  Bundle. 

HOLLOW  MUSCULAR  ORGANS 

resemblance  of  symptoms  in  .         .33 

HOT  DRINKS 

during  an  attack  of  angina  pectoris       53 

HUNTER,  JOHN 

his  description  of  a  curious  attack       26 
his   description    of    Cheyne-Stokes 
respiration  .         .         .         .31 

HYDROTHERAPY      .         .         .       65,296 

HYPERALGESIA 

after  an  attack  of  angina  pectoris  50,  51 

40 

56 

xix 

193 

203 

123 

66 

170 

38 

57 

55 

102 


in  angina  pectoris 

of  breasts        .... 

definition  of    . 

due  to  exhausted  contractility 

due  to  dilatation  of  the  heart . 

in  enlargement  of  the  liver 

extensive  in  neurotic  people    . 

with  the  nodal  rhythm  . 

of  skin  and  muscles  in  gastric  ulcer 

with  valvular  disease 

in  visceral  disease  . 

HYPERPIESIS    . 


INDEX 


407 


IR 


HYPERTROPHY 

of  muscular  coat  of  arteries     . 
of   left   ventricle   in   aortic    valve 
disease        .  .... 

of  right  aui'icle  in  tricuspid  stenosis 

HYSTERIA 

heart  pain  in  . 

INCREASED     PERIPHERAL     RE 
SISTANCE 

a  cause  of  angina  pectoris 

INFANTS    AND    THE    SINUS 
REGULARITY 

INFARCT,  PULMONARY  . 

INFARCTS  DURING  ACUTE  AFFEC 
TIONS  OF  THE  HEART 

INFECTIVE  ENDOCARDITIS  . 
treatment  of  . 

INFLUENZA,    A.-V.    BUNDLE    AF 
FECTED  IN     . 

INQUIRY  INTO  NAUHEIM  TREAT 
MENT 

INSENSITIVENESS    OF   THE   VIS 
CERA 

INSPECTION  OF  THE  ARTERIES 

INSPECTION    OF    THE    JUGULAR 
PULSE      .... 

INSPIRATION,    EFFECT    OF,    ON 
ABDOMINAL  VEINS      . 

INSPIRATORY      SWELLING       OF 
JUGULAR  VEINS  . 

INTERCOSTAL  MUSCLES 
See  Muscles. 

INTERMITTENT  CLAUDICATION  . 

INTERMITTENT  PULSE 

due    to     depression    of    conduc- 
tivity .....     176, 
due  to  depressed  conductivity  in 

febrile  affections 
due  to  exhausted  contractility 
produced  by  digitalis       .         .     186, 
due  to  extra-systoles         .     141,  149, 
in  pneumonia  .... 

sensations  with       .... 

INTERPOLATED  EXTRA-SYSTOLE 

INTERPRETATION  OF  THE  JUGU- 
LAR PULSE     ....     106, 

INTERPRETATION  OF  A  SPHYG- 
MOGRMI 

INTERPRETATION  OF  A  TRACING 
OF  THE  APEX  BEAT  . 

INTERSYSTOLIC  PERIOD 

{a-c  interval)     .    .    .    • 


245 

240 
238 

57 


43 

146 
31 

219 

225 
227 

217 

297 


34 
92 

105 

62 

62 

46 

179 

217 
197 
338 
162 
218 
22 

152 

111 

95 


176 


FAOB 

.  78 
.  82,86,88 

91,  92 
.  251, 276 
THE 


INTERVAL,  PRE-SPHYGMIC 

INVERTED  CARDIOGRAMS 

INVERTED  SPHYGMOGRAM 

IODIDE  OF  POTASSIUM  . 

IRREGULAR     ACTION     OF 
HEART 

classification  of       ...         .     141 

IRREGULAR  HEART 

and  chloroform       ....     263 

IRREGULARITY 

nature  of  disease  shown  by     .         .217 
See  also  Heart  Irregulakity. 

IRREGULARITY    CHARACTERISTIC 
OF  THE  NODAL  RHYTHM  .     118 


FOCUS    IN    SPINAL 


IRRITABLE 

CORD 37,45 

IRRITABLE  HEART  AFTER  RHEU- 
MATIC FEVER 


221 


JAUNDICE 

with  dilatation  of  the  heart     . 
with  heart  failui'e   .         .         .         . 
the  pulse-rate  with 

JUGULAR  PULSE 

airricular  wave  in  the 
aiuicular  depression  in  the 
ventricular  wave  in  the 
ventricular  depression  in  the  . 
the  carotid  wave  in  the  . 
compared  with  auricular  pressure  . 
conditions  giving  rise  to  a 
a  diastolic  wave  in  the    . 
effect  of  dilatation  of  the  heart  on 

the 

effect  of  opening  of  tricuspid  valves 

on  the         .         .         .         .         . 
with  extra-systoles 
factors  producing  the 
graphic  records  of  the 
how  to  record  the  . 
inspection  of  the 


209 
125 
139 

109 
109 
110 
111 
112 
107 
121 
113 

205 

110 
150-159 
.     108 
.     106 
.       68 
.     105 
interpretation  of  the       .         .      106,111 
meaning  of  the  ventricular  form  of 

the 116 

in  mediastino- pericarditis  .  .  245 
period  of  stasis  in  the  .  .  11,114 
with  the  nodal  rhythm  .  1 16,  167,  308 
significance  of  ventricular  form  of 

the 117,238 

standard  for  interpreting  a  .  108,111 
time  of  opening  of  tricuspid  valves 

in  the 80 

in  tricuspid  disease  .         .         ,110 

with  tricuspid  regurgitation  .  1 10,  238 
what  it  shows  ....     105 

variations  of,  due  to  heart's  rate  .  115 
ventricular  form  of  the  .         .         .116 


408 


INDEX 


PAGE 

JUGULAR  VALVE  SOUND     238,  322,  348 

JUGULAR  VEINS 

inspiratory  swelling  of    .         .         .       62 
relation    of,    to    carotid    and    sub- 
clavian arteries  .         .         .         .107 
thrills  produced  by  compression  of     311 

KIDNEY  DISEASE  AND  CARDIO- 
SCLEROSIS       243 

KNOTEN  OF  TAWARA 

See  Aueiculo-Ventriculab  Node. 


LACTIC  ACID 

action  on  tonicity  ...         9 

LEG,  FRACTURE  OF 

and  heart  failure    .         .  27,32,209 

LEG,  DEGENERATION  OF  ARTERIES 


OF 


46 
46 


LEG,  GANGRENE  OF 

LIFE  INSURANCE 

and  the  prognosis  of  symptoms       .  264 

LIVER 

pain  due  to  the       ....  22 

LIVER  ENLARGEMENT 

a  cardinal  symptom  of  heart  failure  122 

effect  of  digitalis  on         .         .         .  286 
in  dilatation  of  the  heart         .      207,  208 

with  nodal  rhythm          .         .         .  170 
pain  and  tenderness  in    .         .      122,  209 

with  paroxysmal  tachycardia          .  207 

signs  of            .....  123 

treatment       .....  128 

LIVER  MOVEMENTS 


in  aortic  regurgitation     . 

241 

due  to  cardiac  aspiration 

83 

ER  PULSATION 

123 

in  adherent  pericardium 

125 

coupled  beats  in      . 

284 

differential  diagnosis  of  . 

126 

distinct  from  liver  movement 

83 

forms  of          .... 

123 

how  to  record 

69 

with  the  nodal  rhythm    . 

123 

prognosis  of    . 

126 

with  paroxysmal  tachycardia 

324 

in  tricuspid  stenosis    .  125,  238,  314,  347 

LUNG,  RETRACTION  OF    .    .   88 

LUNGS 

acute  suffocative  oedema  of  .  .  32 
apoplexy  of  .  .  .  .  .32 
bleeding  from  .         .         .         .31 

displacement  of,  with  dilatation  of 

the  heart 204 

infarct  into  .....  32 
in  the  fixation  of  the  heart      .         .       16 


PAGE 

LUNGS,  OEDEMA  OF       .         .         .  208 

in  the  elderly           ....  27 

factors  in  the  production  of    .         .  210 

first  sign  of     .         .         .         .         .  209 

how  produced         ....  27 

method  of  examining  for         .         .  210 

in  mitral  stenosis    ....  27 
prognostic  significance  of        .         .210 

symptoms  of           ....  210 

in  typhoid  fever      ....  27 

MALIGNANT  ENDOCARDITIS         .  225 

MASSAGE 

in  treatment            ....  295 

MECHANISM    OF    THE    PRODUC- 
TION OF  PAIN       ....  35 

MEDIASTINO-PERICARDITIS 

angina  pectoris  in  .         .         .         .  253 

etiology  of 253 

jugular  pulse  in       ...         .  254 

liver  pulse  in           ....  255 

prognosis  in    .         .         .         .         .  255 

symptoms  of           ....  254 

treatment  of            ....  255 

MEMORY 25 

MENSTRUATION 

nose  bleeding  during       ...         .23 

MENTAL  EXCITEMENT 

a  cause  of  angina  pectoris        .         .  47 

MENTAL  FACTOR 

in  treatment            ....  274 

MENTAL  STATE 

in  Cheyne-Stokes  respiration  .         .  31 

induced  by  heart  abnormalities       .  56 

in  the  X  disease      ....  61 

induced  by  physician's  warnings     .  56 

induced  by  visceral  disease      .         .  55 

MESENTERY,  INSENSITIVENESS  OF  34 

METHOD  OF  DESCRIBING  HEART 

AFFECTIONS           ....  4 

MICTURITION 

after  an  attack  of  angina  pectoris   .  50 

MITRAL  MURMURS 

due  to  acute  endocarditis        .         .  219 

due  to  dilatation     ....  204 
See  also  Murmurs. 

MITRAL  REGURGITATION 

absence  of  angina  pectoris  in  .         .  47 
cessation  of  angina  pectoris   with 

onset  of       .         .         .         .         .47 

in  cardio-sclerosis  ....  235 

causes  of         ....         .  235 

conditions  inducing  heart  failure  in  235 
with  dilatation  of  the  heart    .         47,  235 

murmurs  due  to      .         .         .         .  234 


INDEX 


409 


MITRAL  STENOSIS 

angina  pectoris  in  . 

230 

,234 

causes  of         ...         . 

229 

cerebral  embolism  in 

234 

conditions  inducing  heart  failu 

e  in 

229 

dilatation  of  left  ventricle  in  . 

204 

,230 

delayed  conductivity  with 

229 

haemoptysis  in        .         .         . 

234 

involvement  of  a. -v.  bundle  in 

229 

heart  failure  in        .         .         . 

229 

moderate        .... 

229 

murmurs  due  to      . 

230 

meaning  of  disappearance  of 

pre- 

systolic  murmur  of 

231 

not  an  acute  condition    . 

229 

nodal  rhythm  in      .         .         . 

229 

,233 

paroxysmal  tachycardia  in 

234 

pregnancy  with 

251 

post-mortem  changes  in 

233 

progress  of      . 

232 

a  progressive  lesion 

229 

sclerosis  of  muscle  with  . 

233 

symptoms  in           ... 

232 

systolic  miu-mur  due  to 

232 

MOUTH 

becoming  dry  in  angina  pectoris 

MOVEMENTS  DUE  TO  CAROTID 
PULSE  ...... 

MOVEMENTS  OF  THE  HEART   . 

MOVEMENTS  OF  RESPIRATION 

effect  of,  on  the  pulmonary  circula- 
tion     

MOVEMENTS      IN      TREATMENT, 
SPECIAL 

MURMURS 

due  to  aortic  incompetence     . 

due  to  aortic  stenosis 

amicular  systolic    .... 

cause  of  functional 

in  cardio-sclerosis  .... 

diastolic  mitral,  cause  of 

diastolic,  due  to  mitral  stenosis 

due  to  endocarditis 

meaning  of,  in  acute  conditions 

due  to  mitral  stenosis 

due  to  patent  ductus  arteriosus 

due  to  pericarditis 

presystolic,  character  of 

presystolic,  disappeai'ance  of,  in 
nodal  rhythm      .... 

presystolic,  how  produced 

presystolic,  meaning  of  disappear- 
ance of        ....         . 

presystolic,  position  of  in  cardiac 
cycle  ..... 

presystolic,  separation  of,  from  first 
sound  ..... 

presystolic  tricuspid 


59 


91 
76 


210 

295 

240 
239 
230 
204 
246 
231 
231 
219 
215 
230 
256 
220 
230 

170 
230 

231 

230 

176 

238 


MURMURS  {continued)— 

presystolic,  varying  relation  to  first 

sound  

presystolic  ventricular    . 
significance  of  musical    . 
systolic,  due  to  mitral  regurgitation 
systolic,  due  to  mitral  stenosis 
tricuspid  svstolic    . 

MUSCARIN 

action  on  tonicity 

MUSCLES,  ABDOMINAL 
reflex  stimulation  of 

MUSCLES,  CONTRACTED  IN  GAS- 
TRIC ULCER 

MUSCLE  EXHAUSTION 
a  factor  in  heart  failure 

MUSCLE  FAILURE 
symptoms  in 

MUSCLES,  INTERCOSTAL 

contraction  of,  in  angina  pectoris    . 

MUSCLES,       THEIR       PRIMITIVE 
FUNCTION 

MUSCLES,  SPASM  OF,  A  CAUSE  OF 
PAIN 

MUSCLE,  STERNO-MASTOID 

hyperalgesia  of  . 

MUSCLE  STIMULATION 
in  visceral  disease 

:\IUSCLES,  TONICITY  OF 

MUSCLE,  TRAPEZIUS 

hyperalgesia  of       ...         . 

MUSCLES,  TWITCHING  OF 

in  Cheyne-Stokes  respiration  . 

MUSCULAR  HYPERALGESIA 

consequence   of,   in   liver  enlarge- 
ment ..... 

MUSCULAR  ORGANS 

resemblance  of  symptoms  in  liollow 

MUSCULAR  RHEUMATISM. 
See  Rheumatism. 

MUSICAL  MURxMURS 

significance  of         ...         . 

MYOCARDITIS 

heart-rate  in  ... 

in  acute  fevers 
in  rheumatic  fever 
irregular  action  of  the  heart  in 
symptoms  of  ... 

MYOGENIC  DOCTRINE    . 


368 
232 
219 
234 
232 
237 

9 

37 

38 

235 

207 

41 

38 

4+ 

41 

37 
202 

41 

29 

123 
33 

219 


131 
216 
221 
217 
216 


6 


410 


INDEX 


NAUHEIM  BATHS 


PAGE 

297 


NECK 

pain  in,  during  an  attack  of  angina 
pectoris       .         .         .         .  41,48 

NERVES  OF  THE  HEART 

accelerator     .....       19 
afferent           .         .         .         .         .19 
depressor        .         .         .         .         .19 
effect  of,  on  the  functions  of  muscle- 
fibres  10 

effects  of,  on  the  heart  muscle  .  18 
in  a.-v.  bundle  ....  14 
influence  on  the  heart's  rhythm  .  141 
inhibitory  .  .  .  .  .18 
action  of  sympathetic  ...  18 
origin  of  sympathetic  .  .  .19 
action  of  vagus  .  .  .  .41 
vagus,  effect  of  stimulation  of,  on 

depressed  functions     .         .         .19 
See  also  Vagus. 

NERVES 

diagram    showing   stimulation    of, 

in  visceral  disease 
optic,  stimulation  of 
peculiar   field   supplied   by   upper 

dorsal  .... 

sensory  stimulation  of    . 
sensory,  relationship  of  to  heart 
stimulation  of  trunk  of  . 
sympathetic,  diagram  showing  rela 

tion  to  viscera  and  sensory  nerve 

NERVOUS  SYSTEM 

reaction  of  visceral  disease  on 
hypersensitiveness  of      . 
valvular  disease  with  exhausted 

NEURASTHENIA 

cardiac  ..... 

and  sinus  irregularity 

NEUROGENY     

NEUROSES,  CARDIAC      . 

NEUROTIC  PATIENTS 

treatment  of  . 


36 
34 

40 
36 
40 
35 

36 

55 
55 

57 

56 
146 


56 


.  270 

NITRITE  OF  Al^IYL 

dm-ing  an  attack  of  angina  pectoris       53 

NITRITES  AND  HIGH  BLOOD-PRES- 
SURE         275 

NODAL  BRADYCARDIA  .         .     337 

NODAL  EXTRA-SYSTOLES      .         .     157 

NODAL  RHYTHM 

in  acute  affections  .  .  .  218 
analysis  of  symptoms  of  .  .  309 
with  arterial  degeneration  .  .  103 
artificial  waves  in  tracings  of  .  .311 
auricular  wave  absent  in  apex  trac- 
ings in         .         .         .         .  .81 


NODAL  RHYTHM  {continued)— 

due  to  cardio-sclerosis  .  .  142, 247 
significance  of,  in  cardio-sclerosis  .  248 
illustrative  cases  of  the  .  .  312,  333 
character  of  irregularity  in  .  .  142 
characteristics  of  .  .  .  .117 
classification  of  cases  of  .  .  .  169 
clinical  evidence  of  .         .         .     309 

definition  of  .  .  .  .  xix,  166 
caused  by  digitalis  .         .         .     364 

effect  of  digitalis  in         .       172,  282,  357 
difference  when  due  to  rheumatism 
and  cardio-sclerosis     .         .         .     286 

with  dropsy 208 

effect  of,  on  the  heart's  strength      .     142 


electro- cardiogram  of      .         .      297 

,374 

etiology  of      ....         . 

167 

and  extra-systoles 
experimental  evidence  of 
relation  to  heart-block    . 

164 
120 
185 

cases    illustrating    relation    of    to 

heart-block          .         .         .336 

,364 

laboured  breathing  in     . 

27 

and  liver  pulsation 

in  mitral  stenosis    .         .         .      230 

127 
,233 

causing  paroxysmal  tachycardia     . 
pathology  of            .... 

172 
310 

in  pneumonia          .... 
and  pregnancy        .... 
pulsation  of  the  liver  with  the 
character  of  pulse  in        .         .         . 

218 
260 
123 
167 

due  to  advanced  rheumatic  disease 

142 

signs  of  danger  in  . 
starting-place  of     . 

172 
142 

susceptibility  of,  to  digitalis    . 
transient         ..... 

282 
172 

ventricular  form  of  venous  pulse 

in 

118 

See  also  Heakt  Irregularity. 

NORMAL  VENOUS  PULSE. 

See  Jugular  Pulse. 

NOSE  BLEEDING 

at  menstrual  period         ...       23 
in  aortic  disease      ....       23 

NOURISHMENT  OF  HEART  MUSCLE 

angina  pectoris  due  to  impaired      .       43 

NUTRITION 

exhaustion  of  contractility  due  to 
imperfect    .         .         .         .         .192 

OBSCURE  CASES 

prognosis  in    .         .         .         .         .     267 

OEDEMA.     See  Dropsy. 

OEDEMA  OF  THE  LUNGS 
See  Lungs. 

OEDEMA,  PULMONARY.     See  Lungs. 

OLD  AGE 

viscero-motor  reflex  in    .         .         .41 


INDEX 


411 


OPIUM 

PAGE 

.     270 

in  angina  pectoris 
in  cardio-sclerosis   . 

.       54 
.     251 

OPPRESSION  OF  THE  CHEST 

in  the  elderly 

.     130 

OPTIC  NERVE 

stimulation  of         .         .         . 

.       35 

ORIGIN  OF  MISTAKEN  DIAGNOSES  215 

OVER-EXERTION 

causing  angina  pectoris  ...  42 

OVERSTRAINED  HEART         .        .  132 


OXYGEN 

in  angina  pectoris 
in  cardiac  asthma 
in  treatment 


54, 279 
29,  279 

.     278 


PAIN 

absence  of,  in  pericarditis        .         .     220 
in  aneurysm  ....     252 

in  angina  pectoris,  region  of    .         40,  48 
persisting  after  an  attack  of  angina 

pectoris       ..... 
of  biUary  colic,  situation  of     . 
due  to  exhausted  contractility 
function  of      . 

in  gastric  ulcer        .... 
of  heart  affections,  reasons  for  in 

arm    ...... 

of  heart  aflfections,  situation  of 

of  herpes  zoster,  simulating  angina 

pectoris 

over  the  liver  .... 

in  enlargement  of  the  liver 

mechanism  of  its  production 

due  to  peristalsis  of  the  bowel 

radiation  of    . 

of  renal  colic,  situation  of 

significance  of         ...         . 

situation  of     . 

caused  by  spasm  of  hollow  muscles 

vague  notion  of  position  of 

why  it  is  referred    .... 


50 
38 
193 
38 
38 

39 
39 

57 

22 

122, 209 

.   35 

.   34 

22 

'.      39 

.   22 

.   22 

44 

21 

38 


PALPITATION 22 

definition  of  .  .  .  .  xix,  134 
heart-rate  in  .  .  .  .  .134 
and  paroxysmal  tachycardia,  dis- 
tinction between  .  .  .  134 
sensation  during  .  .  .  .135 
sign  of  exhausted  contractility        .     193 

PARALYSIS  OF  THE  AURICLE 

evidences  of    .         .         .         •         .117 

PAROXYSMAL  TACHYCARDIA 

of  auricular  origin  .         .         •     334 

a.-v.  node  affected  in  cases  of .      324,  328 
in  cardio-sclerosis  ....     247 


PAROXYSMAL  TACHYCARDIA 

(continued) — 
cases  illustrating     . 
definition  of   . 

dilatation  of  the  heart  with     . 
liver  enlargement  in 
liver  pulsation  during     . 
meaning  of  the  term 
in  mitral  stenosis    . 
and  palpitation,  distinction  betw 
pathology  of  .         .       310, 

primitive  cardiac  tissue  in 
prognosis  in    . 
pulsus  alternans  due  to  . 
symptoms  of  ... 

sudden  relief  on  cessation  of   . 
sudden  changes  due  to    . 
treatment  of  ... 

PATENT  DUCTUS  ARTERIOSUS 
murmm's  of    . 

PATENT  FORAMEN  OVALE    . 


320-336 

xix,  134 

.     207 

127, 208 

.     324 

134, 172 

.     234 

een    134 

324, 328 

324, 328 

.     173 

198, 335 

.     172 

.     207 

.     207 

.     173 


256 


156 


PATHOLOGY  OF  HEART 

in  angina  pectoris  .  .  304,  305,  353 
in  cardio-sclerosis  245.  328,  353,  355 

in  nodal  rhythm  .  .  '  .  168,310 
in  paroxysmal  tachycardia  310,  324,  328 
shown  by  irregularity    .         .       140, 217 

PATHOLOGICAL  VENOUS  PULSE. 
See  Ventricular  Jugvlar  Pulse. 

PATIENT 

position  assumed  by  .  .  .20 
preliminary  examination  of  .  .  20 
respiration  of  ....       20 

sensations  of  .  .  .  .  .20 
sensations  of  a  guide  to  condition 

of  reserve  force   .         .         .         .21 
necessity    for    precision    in    state- 
ments of     .         .         .         .         .21 

PATIENT'S  APPEARANCE       .        .       20 

PATIENT'S  GAIT       ....      20 

PATIENT'S  HISTORY       .         .        .20 

PECTINATE  FIBRES  OF  AURICLES 

their  function  and  position     .         .       16 

PENIS 

ram's  horn 212 

PERICARDIAL  ADHESIONS 

after  rheumatic  fever      .         .         .221 

PERICARDIAL  EFFUSION 

embarrassing  the  heart  .  .  .  220 
simulating  dilatation  .  .  203, 204 
symptoms  of  ....     220 

PERICARDIAL  SAC 

in  the  fixation  of  the  heart      .         .        16 


412 


INDEX 


PERICARDITIS 

in  acute  fevers  .  .  .  .214 
a  misleading  term  .         .         .     215 

a  painless  affection  .         .         .     220 

symptoms  of  ....     220 

See  also  Mediastino-Pericarditis. 

PERICARDIUM 

adlierent  .....  252 
insensitiveness  of  .  .  .  .34 
in  rheumatic  fever  .         .         .221 

PERIODIC  RESPIRATION        .         .       31 

PERIPHERAL  RESISTANCE 

effect  of  increased  .         .         .     102 

PERISTALSIS 

of  the  bowel,  pain  caused  by  .         .       34 

PERITONEAL  ADHESIONS 

insensitiveness  of    .         .         .         ,34 

PERNICIOUS  ANAEMIA 

epigastric  pulsation  in     .         .  .85 

jugular  pulse  in       ...  .     121 

laeart-rate  in  .         .         .  .130 

PERSPIRATION 

during  an  attack  of  angina  pectoris       48 

PETIT  MAL  .         .         .24, 25, 343 

PHYSIOLOGICAL  VENOUS  PULSE 

See  Auricular  Jugular  Pulse. 

PLATEAU,  SYSTOLIC 

in  apex  tracing      .         .         .     78,  80,  82 

PNEUMONIA 

case  illustrating  severe  heart  affec- 


tion  in 

.     223 

the  heart  in    . 

214, 223 

hypostatic 

.     209 

irregular  heart  in 

.     224 

nodal  rhythm  in 

.     218 

pericarditis  in 

.     221 

the  pulse  in    . 

.     223 

pulsus  alternans  in 

197,218 

POLYGRAPH 

the  clinical 

.       68 

the  ink   . 

.       72 

POLYSEROSITIS 

.     252 

POSITION    OF    THE 

HEART    IN 

DILATATION  . 

.     204 

POST-MORTEM  RECORDS  OF  CASES 

of  angina  pectoris  .  .  304,  305,  353 
of  cardio-sclerosis  .  .  328,  353,  355 
of  nodal  rhythm       .     314,316,318,349, 

[324,  328 
of  paroxysmal  tachycardia  .  324, 328 
of  pulsus  alternans         .         .      353, 355 

POWER  OF  RECOVERY 

a  basis  for  prognosis        .         .         .     265 


PREGNANCY 

jugular  pulse  in 
heart-rate  increased  in    . 
slow  pulse-rate  in  . 
and  oedema  of  the  lungs 


121 
132 
139 

209 


PREGNANCY  AND  HEART  DISEASE 

importance  of  the  subject       .         .  258 

management  of  the  labovir      .         .  260 

standards  for  guidance   .         .         .  258 

signs  of  danger  in  mitral  disease      .  259 

signs  of  danger  in  aortic  disease      .  259 

signs  of  danger  in  dilatation    .         .  259 
signs    of    danger    with    the    nodal 

rhythm 260 


PRESPHYGMIC  INTERVAL     . 
PRESSURE.    See  Arterial  Pressure. 


78 


PRESYSTOLIC  MURMUR 

varying  position  of  in  cardiac  cycle  231 
varying  relation  to  first  sound  .  368 
See  also  Murmurs. 


PRESYSTOLIC  THRILL 

the  first  sign  of  mitral  stenosis 

PRIMARY  WAVE 

in  a  sphygmogram 

PRIMITIVE  CARDIAC  TISSUE 
in  cardio-sclerosis 
cases  illustrating  pathology  of 
and  extra-systoles 
functions  of    . 
in  the  mammalian  heart 
affected  in  the  nodal  rhythm  . 
the    starting-place    of    the    heart's 
contraction  in  the 


.  230 

.   96 

.  248 

312,315 

162 

151 

13 

311 


PRIMITIVE  CARDIAC  TUBE  . 
function  of      . 


11, 141 

11 
141 


PROGNOSIS 264 

in  angina  pectoris  ....  50 
basis  for  ....      265,294 

in  cardio-sclerosis  .         .         .     248 

in  cases  with  exaggerated  sensory 

symptoms  .....  63 
in  Cheyne-Stokes  respiration  .  .  30 
in  depression  of  conductivity  .  .189 
in  congenital  affection  of  the  lieart  257 
in  exhaustion  of  contractility  .     198 

dangers  of  ignorance  in  giving  a  .  264 
in  dilatation  of  the  heart  .  .211 
use  of  digitalis  in  .  .  .  .  212 
of  extra-systoles  ....  164 
effect  of  a  gloomy  .         .     264, 275 

the  field  of  cardiac  response  in  .  265 
in  heart-block  .  .  .  .189 
and  life  insurance  .         .         .     264 

in  liver  enlargement  .  .  .  126 
importance  of  ...         .     264 

in  increased  heart-rate    .         .         .     136 


INDEX 


413 


PAGE 

PROGNOSIS  {rontinued)— 

in  mediastino-pericarditis  .  .  255 
in  the  nodal  rhythm  with  increased 

rate 169,  171 

in  obscure  cases      ....  267 

in  paroxysmal  tacliycardia  .  .  173 
of  the  pulsus  alter  nans    .         .         .198 

the  reserve  force  in          .         .         .  266 

responsibility  of  giving  a         .         .  264 

of  sinus  irregularities      .         .         .  146 

in  syncope      .....  266 

in  typhoid  fever      ....  210 

in  valvular  affections      .         .         .  242 

PROGRESSIVE  NATURE 

of  valvular  sclerosis         .         .         .     229 

PROTECTION 

the  function  of  contracted  muscles  37 
the  function  of  pain        ...       37 

PROTECTIVE  MECHANISM 

angina  pectoris  a  .  .  .  .45 
in  gastric  ulcer  ....  38 
in  joint  disease  ....  38 
reflex      ......       33 

PSEUDO-ANGINA  PECTORIS 

a  useless  and  misleading  term  .     56 

PSOAS  ABSCESS 

and  the  heart- rate  .         .         .133 

PUERPERAL  FEVER 

a.-v.  bundle  affected  in  .  .  .  217 
the  heart  in 226 

PULMONARY  ARTERY 

tracings  from      ....     78,  79 

PULMONARY  CIRCULATION 

effect  of  respiratory  movements  on    210 

PULMONARY  STASIS,     ^ee  Lungs. 

PULMONARY  VEINS 

heart's  contraction  starting  at         .       13 

PULSATION 

causes  of  epigastric .         .         .        83,  85 

PULSATION,  CAPILLARY 

in  aortic  regurgitation    .         .         .241 

PULSE 

anacrotic        .....  240 

in  aortic  incompetence    .         .         .  240 

in  aortic  stenosis     ....  239 

in  angina  pectoris  ....  302 
character  of  irregularity  in  nodal 

rhythm       .....  167 

causes  of  unequal  radial          .         .  94 

Corrigan's       .....  240 

digital  examination  of  arterial  .  90 
effect  of  auricular  contraction  on 

radial 184 

liver       ......  123 

how  to  record  liver          ...  69 


PULSE  {continued)— 

intermission  due  to  depressed  con- 
ductivity    ....     176, 179 
intermission  due  to  extra-systoles 

141, 149 
nature  of  movements  of  arterial  .  91 
not  due  to  expansion  of  the  artery  91 
in  palpitation  .... 

in  pneumonia  .... 

rate,  classification  of  diminished 
rate,  slow,  due  to  heart- block 
rate,  slow,  due  to  true  bradycardia 
rate,  reckoning  of  the 
rate  during  syncope 
rhythm  of  the  .... 

slow,  due  to  feeble  contraction  of 
ventricle     ..... 
water-hammer        .... 
wave,  impact  of  the 
wave,  size  of  .... 


what  is  it  ? 


135 
223 

138 
138 
139 

93 
187 

94 

138 

.     240 

94 

94 

90,  92 


PULSE,  VENOUS.    -See  Jugular  Pulse. 


PULSUS  ALTERNANS       . 

in  acute  affections  of  the  heart 


43,  50,  196, 


194, 196, 
.      194, 

xix, 
.      197, 


196, 


in  angina  pectoris 
and  arterial  pressure 
with  cardiac  asthma 
in  cardio-sclerosis  . 
causation  of  . 

conditions  giving  rise  to  tlie    . 
definition  of    . 
due  to  digitalis 

distinct  from  extra-systoles    . 
distinct  from  pulsus  bigeminus 
with  extra-systoles 
field  of  response  with 
frequency  of  ... 

heart  sounds  with   . 
how  produced 

with  paroxysmal  tachycardia 
in  pneumonia  .         .         .         . 

prognosis  of    . 

significance  of         ...         . 
significance  of,  in  cardio-sclerosis    . 
a    symptom    of    exhausted    con- 
tractility    ,         .         .         .         . 


198, 


142 
197 
303 
196 
29 
248 
350 
197 
194 
288 
198 
198 
350 
196 
196 
198 
194 
335 
197 
198 
194 
248 

194 


PULSUS  BIGEMINUS 

definition  of   . 

heart  sounds  in  .  .  • 
distinct  from  pulsus  alternans 
due  to  extra-systoles 

PULSUS  BISFERIENS 
in  aortic  stenosis     . 

PULSUS  CELER 

PULSUS  PARADOXUS 

in  mediastino-pericarditis 

PULSUS  TARDUS      . 


xix,  149 
.  150 
.  198 
.     141 


240 
94 


254 
94 


414 


INDEX 


PAGE 

PURKINJE  FIBRES  ...       14 

PURPOSE  OF  VISCERAL  REFLEXES     37 


PYAEmA 

heart  in 


RADIAL  PULSE 

as  a  standard 
causes  of  unequal 


226 


75 
94 


RECURRENT  ATTACKS 

of  angina  pectoris            ...  50 

REFLEX  PROTECTIVE  PHENOMENA 

in  visceral  disease            ...  33 

REFLEX  SYMPTOMS 

dui'ing  an  attack  of  angina  pectoris  48 
cause  of  exaltation  of      .         .         .38 

in  dilatation  of  the  heart         .         .  202 

due  to  exhaustion  of  contractility  .  193 
in  enlargement  of  the  liver      .         .122 

exaggerated  in  neurotic  people        .  -  55 

REFLEX,  VISCERO-MOTOR     .         .  37 

REFLEX,  VISCERO-SENSORY         .  35 

in  angina  pectoris            ...  40 

REFLEXES,  VISCERAL,  PURPOSE 

OF 37 

REGURGITATION 

into  coronary  sinus,  how  prevented  16 

into  veins,  how  prevented       .         .  16 

RENAL  COLIC.     See  Colic. 

RESECTION  OF  BOWEL 

in  conscious  subject        ...  34 

RESERVE  FORCE     ....  2 

conditions  exhausting  the       .         .  3 

of  the  function  of  contractility        .  192 

in  prognosis    .....  266 

restored  by  training        .         .         .  266 
increased  heart-rate  with  exhaustion 

of 130 

See  also  Heart  Muscle.  t 

RESPIRATION 

effect  of  movements  of,  in  the  pul- 
monary circulation      .         .         .  210 
causing  irregular  heart-action          .  143 
slow,  due  to  digitalis       .         .         .31 
slow,  inducing  irregular  action  of 

the  heart    .         .         .         .         .31 

slow  and  vagus  stimulation     .         .  31 

RESPIRATORY  SYMPTOMS     .         .  26 

RESPONSE,  FIELD  OF 

in  heart-block         ....  187 

the  standard  of  heart's  strength      .  4 


PAGE 

REST 

effect  of,  on  depressed  conductivity 

177, 180 

importance  of,  in  exhausted  con- 
tractility    ..... 

in  treatment  .... 

want  of,  a  cause  of  exhaustion  of 
the  heart    ..... 

want  of,  a  cause  of  angina  pectoris 

RESTLESSNESS 

treatment  of  .... 


199 
269 

46 
46 


270 


RETRACTION  OF  STRUCTURES 


due  to  ventricular  systole 

.       81 

RETROGRADE  EXTRA-SYSTOLE  .     160 

RHEUMATIC  FE\T:R 

affection  of  a. -v.  bundle  in 

185, 217 

cellular  foci  in  heart  muscle  in 

.     221 

dilatation  of  the  heart  in 

.     222 

extra-systoles  in 
heart  in  . 

.     218 
214,  221 

heart  symptoms  in 
irritable  heart  after 

.     222 
.     221 

mitral  stenosis  due  to 

.     229 

pericardial  adhesions  after 
pericarditis  in          .         .         . 
slow  cicatrization  in  heart  after 

.     221 
.     220 
.     221 

RHEUMATIC  HEART 

exhaustion  of  contractility  in 


193 


RHEUMATIC  HEART  CASES 

dropsy  in 209 

RHEUMATIC  AFFECTION  OF  THE 
HEART     ♦ 

causing  the  nodal  rhythm       .      1-12,  168 

RHEUMATIC  HEART  ^^^TH  THE 
NODAL  RHYTHM 

effect  of  digitalis  on        .         .         .     172 

RHEUMATISM,  MUSCULAR 

contraction  of  intercostal  muscles  in      41 

RHYTHmCAL  CONTRACTION  OF 
THE  HEART 

cause  of  .....         8 

RIBS 

resection  of,  in  adhesive  medias- 
tinitis 255 

RIGHT  VENTRICLE 

and  epigastric  pulsation  •        .         .       85 

RIGHT  VENTRICLE  CAUSING  THE 
APEX  BEAT 85 

RUPTURE  OF  AORTIC  VALVES  .     239 

RUPTURE  OF  THE  HEART  .         .     202 
with  arterial  degeneration       .         .     103 


INDEX 


415 


S.-A.  NODE. 

See  SiNO-AuRicuLAR  Node. 

SALICYLATE  OF  SODA 
in  rheumatic  fever  . 


PAGE 


223,  277 


SALIVA,  INCREASED  SECRETION  OF 
in  angina  pectoris    .         .         .         42, 48 

SALT 

in  angina  pectoris   .        .         .         .53 
in  dropsy        .....     212 

SCHOOLBOYS 

and  the  sinus  irregularitj^        .         .     146 

SCLEROSIS  OF  MUSCLE 

with  mitral  stenosis         .         .         .     233 

SCLEROSIS      OF      VALVES      AND 
HEART  MUSCLE 

association  of  ....     229 

SCLEROTIC  CHANGES 

progressive  nature  of      .         .         .     229 

SEA-BATHING    ....       65,296 

SEGMENTATION  OF  THE  BODY 

cause  of  .....       38 

SENILE  HEART      ...  243 

oedema  of  the  lungs  with        .         .     209 
symptoms  caused  by  the         .         .130 

SENSATIONS  OF  PATIENTS 

during   an   attack   of   heart-block 
syncope       .....     188 

SENSE  OF  EXHAUSTION        .         .       22 

SENSE  OF  niPENDING  DEATH 

in  angina  pectoris  ...       49 

in  palpitation  ....     135 

SENSORY  NERVE.     See  Nerve. 

SENSORY  PHENOMENA 

in  cardio-sclerosis  ....       58 
in  nervous  people   ....       59 

SEPTIC  INFECTIONS 

a.-v.  bundle  affected  in  . 
the  heart  in    . 
heart-block  in 


SEPTUM,  A.-V. 

action' of  muscles  on 


SHOCK    DUE    TO    VENTRICULAR 
SYSTOLE  .         .         .         .        87,89 

SINO-AURICULAR  NODE 

constitution  of        .         .         .         .14 

definition  of  term xix 

position  of      .         .         .         .         .14 
the   starting-place   of   the   heart's 
contraction  ....     141 


PAGE 

SINUS  IRREGULARITIES  .  141,  143 
character  of  .  .  .  .  .  140 
in  healthy  people  ....  146 
and  the  X  disease  .  .  .  .146 
See  also  Heart  Irregularity. 

SINUS  VENOSUS  ....  14 
formation  of  .  .  .  .  .13 
in  the  mammalian  heart  .         .       13 

starting-place  of  the  heart's  con- 
traction      .....     140 

SKIN,  ATTENUATION  OF 

due  to  obliteration  of  capillaries 

SKIN,  HYPERALGESIC 

after  an  attack  of  angina  pectoris 


.     217 

214,  225 

.     217 

.       16 


SLEEP 

angina  pectoris  induced  by  want  o 
with  cardiac  asthma 
Cheyne-Stokes  respiration  during 
importance  of,  in  treatment    . 
necessity  for,  in  cardio-sclerosis 
necessity  for  inquiry  into 

SLEEPLESSNESS 

inducing  angina  pectoris 

SLOW  BREATHING  . 


244 

51 

250 

28 

29 

269 

250 

21 

,  270 
31,62 


SLOWING  OF  THE  WTIOLE  HEART 
by  digitalis     .....     367 

SLOW  PULSES 

classification  of       ...         .     138 

SODIUM  SALICYLATE 

Lee's  method  of  using     .         .         .     277 

SOLDIER'S  HEART  .         .        .        .131 

SOLDIERS 

sinus  irregularity  in  healthy    .  •      .     146 

SOUND     CAUSED     BY     VENOUS 


VALVES    

SOUNDS  OF  THE  HEART 

in  cardio-sclerosis  . 
due  to  extra-systoles 
in  nodal  rhythm 
in  sinus  irregularity 

SOUTHEY'S  TUBES 

in  the  treatment  of  dropsy 

SPAS 

treatment  at  ... 

cause  of  efficacy  of  treatment  at 

SPASM  OF  THE  HEART 

impossible      .... 

SPASM  OF  HOLLOW  MUSCLES 
a  cause  of  pain 

SPHYGM0GRA3I 

definition  of    . 
diastolic  notch  in  a 
diastolic  period  in  a 


322, 348 


142 


246 
150 
232 
145 

212 

296 
299 

44 

44 

95 
96 
96 


416 


INDEX 


PAGE 

SPHYG:\I0GRA^I  (continued)— 

diastolic  wave  in  a  .  .  .96 

instrumental  defects  in  a  .  .97 

interpretation  of  a  .  .  .95 

inverted  .         .         .  .  91, 92 

the  primary  wave  in  a     .  .  .       96 

systolic  period  in  a  .  .  .95 

tidal  wave  in  a        .         .  .  .96 

the  value  of  a  .         .  .  .94 

SPHYGMOGRAPH,  THE   ...       67 

SPINAL  CORD 

diagram  showing  relation  to  sensory 

nerve  .....       36 

effect  of  reflex  stimulation  on  .       45 

irritable  focus  in     .         .         .  37, 45 

irritable,  in  visceral  disease     .         .       37 

SQUILLS 281,291 

STAIRCASE  PHENOMENON 

produced  by  digitalis      .         .         .     367 

STANDARDS 

for  recognizing  events  in  a  cardiac 
revolution  .....       55 

STANDPOINT 

from  which  this  book  is  written       .         5 

STANDSTILL  OF  HEART 

due  to  digitalis        ....  367 

in  nodal  rhythm     ....  345 

in  sinus  irregularity         .         .         .  146 

in  vagus  stimulation       .         .         .  145 

STANNIUS  LIGATURES    .         .       13,  141 

resemblance  of,  to  heart-block         .     187 

STARTING-PLACE 

of  heart's  contraction 
of  the  nodal  rhythm 

STASIS,  PULMONARY.     See  Lungs 

STATUS  LYJ^IPHATICUS 
and  chloroform 

STERNO-MASTOID.    See  Muscles. 

STIMULANTS 

danger  in  the  use  of 

STIMULI,  SUMMATION  OF 
and  angina  pectoris 

STIMULUS  PRODUCTION 
and  angina  pectoris 

STROPHANTHUS       . 


13 
142 


262 


66 


43 

7 
43 

291 


STRYCHNINE  . 

of  little  use  in  treatment      v~:i  ^^. 

SUFFOCATION,  SENSATION  OF     . 

in  Cheyne-Stokes  respiration  . 
a    symptom    of    exhausted    con- 
tractility    ..... 

SUFFOCATIVE  OEDEMA  OF  LUNGS 


PAGE 

SUGGESTION  IN  TREATMENT       .       64 

SULPHONAL       ....     251,270 

STOIMATION  OF  STIMULI 

a  cause  of  angina  pectoris        .         .       43 

SURGICAL  OPERATIONS 

how  arteries  recognized  in       .         .91 

SWALLOWING 

effect  of,  on  conductivity  .  .     362 

stimulates  the  vagus       .  .  .186 

effect  of,  on  the  heart      .  .  .144 

SYMPATHETIC  FIBRES 

in  s.-a.  node    .....       13 

SYMPATHETIC  NERVES. 

See  Nerves  of  the  Heart. 

sy:\iptoms 

classification  of,  in  visceral  disease  33 

due  to  changes  in  organs  .  .  33 
nature    of,    produced    by    hollow 

muscular  organs  ...  33 
of  heart  affection,   confusing  and 

contradictory      ....  5 

due  to  impaired  function  of  organs  33 

due  to  nerve  reflexes       ...  33 

.  23 

.  186 

.  225 

.  187 

.  188 

.  266 

.  146 


277 

27 
30 


193 
32 


SYNCOPE    

due  to  digitalis 

fatal  in  diphtheria 

due  to  heart-block 

pulse- rate  during    . 

prognosis  in    . 

with  sinus  irregularity    .    '     . 

SYPHILIS     AND     CARDIO-SCLER- 
OSIS 244 

SYPHILITIC  GUMMATA 

causing  heart-block         .         .         .     185 

SYSTOLIC  PERIOD 

in  a  cardiogram  ....  78 
in  a  phlebogram  .  .  .  .110 
in  a  sphygmogram  ...       95 

TACHYCARDIA 

loose  employment  of  term       .         .       56 

See  Heart-Rate. 

See  Paroxysmal  Tachycardia. 

TAENIA  TERMINALIS 

contraction  of,  prevents  regurgita- 
tion into  veins     .         .         .         .16 
in  ventricular  jugular  pulse     .         .     118 

TEMPERATURE 

relation  of,  to  pulse-rate  .         .     215 

TENDERNESS 

in  enlargement  of  the  liver      .         .     122 

THEOBROMINAE  SODII  SALICYLAS  212 
THEOCIN-SODIUM  ACETATE  .     212 


INDEX 


417 


PAGE 


THRILL 

due  to  aortic  stenosis       .         .         . 
due  to  compression  of  jugular  vein  . 
due  to  mitral  stenosis      .         • 
due  to  patent  ductus  arteriosus 

TIDAL  WAVE 

in  a  sphygmogram 

TONICITY  .         . 

function  of  . 
and  angina  pectoris 
effect  of  digitalis  on 
effects  of  drugs  on  . 
functional  murmur  caused  by  de- 
pression of  ■  •  •  ■ 
importance  of,  in  the  nodal  rhythm 
symptoms  of  depression  of 

TORTUOUS  ARTERY 

nature  of  movements  of  .         'JI 

TRACINGS 

how  to  take 


239 
311 
•230 
256 

95 


70 


TRAINING 

reserve  force  restored  by 

TRANSIENT  NODAL  RHYTHM. 
See  Paroxysmal  Tachycardia. 

TRAPEZIUS.     See  Muscle. 

TREATMENT      .         •         •         •        j^ 

of  angina  pectoris  .         .         '  .     Z^'" 
of  acute  febrile  conditions  of  the 

heart  ..••■• 
of  cardio-sclerosis  .  .  •  • 
of  cases  with  exaggerated  sensory 

symptoms  .         .         ■         •         • 
of  Cheyne-Stokes  respiration  . 
of  congenital  affections  of  the  heart 
of  exhausted  contractility 

of  dropsy 

bearing  of  dilatation  on  . 
of  dilatation  of  the  heart 
of  extra-systoles     . 
of  exophthalmic  goitre    . 
of  heart  failure  with  dropsy    . 
of  high  arterial  pressure 
of  heart-block  .         •         • 

with  enlargement  of  the  liver  . 
of  mediastino-pericarditis 
of  neui-otic  patients         .         •         • 
of  nodal  rhythm  with  no  increase  in 
rate     .••••• 
of  the  nodal  rhythm  with  increased 

rate    ..•■•■ 
of  oedema  of  the  lungs    . 
of  paroxysmal  tachycardia      . 
of  cases  sho^ving  the  pulsus  alter- 


266 


65, 


nans   . 
of  valvular  affections 
aperients  in    . 
ammonium  bromide  in 

JIACKENZIE 


06, 134 


226 

249   [ 

64 

30 
257 
199 
211 
207 
211 
164 
134 
272 
103 
190 
128 
255 
270 

170 

171 
213 
173 

199 
242 
273 

.270 


in 


TREATMENT  (continued)— 

baths  in  .... 

bodily  comfort  in    . 

deep  breathing  in   .         •      .  ■      ' 

the  condition  of  the  bowels  in 

essential  principle  in 

digitalis  in      ...         • 

drugs  in  .... 

diet  in  .... 

enemata  in      . 

rules  for  employment  of  exercise 

food  in   . 

hypnotics  in   .         .         .         ■ 

harm  of  injudicious  feeding  in 

massage  in      .         .         •         ■ 

importance  of  mastication  in  . 

milk  in 

the  mental  factor  in 

Nauheim         .         ■         •         ■ 

oxygen  in 

position  assumed  by  patient  in 

by  position     .         •         •         • 

rest  in     . 

sea-bathing  in         .         .         • 

I  sleep  in  . 

I  at  spas   .         .         .         •         • 

j  cause  of  efficacy  of  spa    . 

by  special  exercises 
by  special  movements     . 

I  by  suggestion 

vaso-clilators  in       . 
venesection  in         .         •         • 

TRICUSPID  REGURGITATION 

I  effect  on  the  jugular  pulse 

a  normal  condition 
j  without  a  murmur 

I  and  the  venous  pulse 

TRICUSPID  STENOSIS 

cases  of  .         .         • 
pulsation  of  liver  in 
sound  of  jugular  valves  in 
symptoms  of  . 

TRICUSPID  SYSTOLIC  MURMUR 
position  of      .         •         •         •         • 

TRICUSPID  VALVE  DISEASE 

jugular  pulse  in       .         •         •         • 

TRICUSPID  VALVES 

effect  of  opening  of,  on  the  jugular 
pulse  •         •         •         •         • 

TUBE 

primitive  cardiac    .         •         •         • 

TUBERCULAR  MENINGITIS 
periodic  respiration  in     . 
sinus  irregularity  in 

TUBERCULOSIS 

heart-rate  increased  in    . 


PAGE 

.  296 
.  270 
210,  213 
.  274 
.  268 
.  212 
.  274 
.  271 
.  274 
293 
.   66 
.  270 
.  271 
.  295 
.  271 
.  271 
.  274 
.  297 
.  278 
.  271 
.  212 
.  269 
65, 296 
.  269 
.  296 
.  299 
.  295 
.  295 
64, 274 
.  275 
.  293 


110 
237 
237 
238 


315, 
125, 


346 
238 
238 

238 


237 
110 

110 
11 


31 

146 


132 


E  e 


418 


INDEX 


TYPHOID  FEVER 

epigastric  pulsation  in 
the  heart  in    . 
heart  failure  in 
heart- rate  in  . 


84 
214 
•210 
130 


prognostic  sign  of  oedema  of  tlie 

lungs  in 210 

rapid  breatliing  in  .         .         .         .27 


ULCER,  GASTRIC 

contracted  muscles  in 
hyperalgesia  in        .         .         . 
meaning  and  pui'pose  of  symptoms 

in        ....         . 
pain  in 

ULCERATION  OP  MITRAL  VALVES 


38 
38 

38 
38 

221 


UMBILICAL  REGION 

cause  of  pain  in       .         .         . 

UNCONSCIOUSNESS 

due  to  angina  pectoris    . 

URETER 

nature  of  symptoms  produced  by 

URINE 

increased  secretion  of,  during  an 

attack  of  angina  pectoris      .         42,  48 
secretion  of,  in  dilatation  of  the 

heart  ..... 

diminished  secretion  of,  with  dropsy 
significance  of  diminished  secretion 

of 210 

secretion  of,  in  dilatation  of  the 

heart 210 

UTERUS 

natui'e  of  symptoms  produced  by  . 

VAGUS  NERVE 

in  s.-a.  node    ..... 

VAGUS  SENSORY  REFLEX     . 

VAGUS  STIMULATION 
causing  slow  respiration 
by  deep  breatliing 
in  experiment         .... 
in  heart-block         .... 


34 


49 


33 


206 

208 


33 


13 

41 

31 
144 
145 

186 


by    swallowing,    producing    heart- 
block  362 

by  swallowing         .         ,         .      140,  186 
producing  sinus  ii'regularities  .     146 

VALVE  DEFECTS 

associated  with  sclerosis  of  heart 

muscle 229 

the  manner  of  heart  failure  due  to     228 

VALVES 

opening  of  auriculo- ventricular       ,       81 

VALVULAR  DISEASES 

and  angina  pectoris         ...       57 
and  arterial  pressure       .         .         .      103 


PAGE 

VALVULAR  DISEASES   (continued)— 

and  chloroform       ....  261 

with  hyperalgesia   ....  57 

and  exhausted  nervous  system        .  57 

heart-rate  increased  in    .         .         .  131 

prognosis  in    .         .         .         .         .  242 

reflex  symptoms  exaggerated  in      .  57 

treatment  of  .         .         .         .         .  242 

VALVULAR  SCLEROSIS 
progressive  natirre  of 

VASO-CONSTRICTORS 
in  treatment 

VASO-DILATING  DRUGS 
in  angina  pectoris  . 
in  high  arterial  pressui-e 


229 

276 

54 
104 
275 


in  treatment 

VASOMOTOR  ANGINA  PECTORIS  49,  62 

VEGETATIONS  IN  ACUTE  RHEU- 
MATISM   221 

VEGETATIONS  ON  VALVES 

after  confinement  ....  225 
symptoms  of  ....     219 

VEINS 

heart's  contraction  starting  at  the 

mouths  of  .  .  .  .  .16 
how  regmgitation  into  is  prevented  16 
in  the  fixation  of  the  heart      .         .       16 

VENESECTION 

indications  for         ....     292 

VENOUS  PULSE.    See  Jugular  Pulse. 

^^NTRICLE 

action  of  pectinate  fibres  on  .  .  16 
coui'se  of  dilatation  of  left,  in  mitral 

stenosis       .....     203 
exhaustion  of  the  left,  a  cause  of 
angina  pectoris   ....       46 

filling  of 81 

fixation  of  the  ....  16 
perception  of  contraction  of  .  .76 
period  of  contraction  of  .  .  .78 
period  of  filling  of  .  .  .  .81 
period  of  relaxation  of    .         .         .80 

VENTRICULAR  CONTRACTION 

electro-carcUogram  of     .         .         .     373 

\TENTRICULAR  FALL 

in  a  jugular  pulse    .         .         .     109,111 

VENTRICULAR  EXTRA-SYSTOLE .     151 


VENTRICULAR  HYPERTROPHY 
in  aortic  valve  disease     . 


239 


VENTRICULAR  JUGULAR  PULSE     116 

auricular  hypertrophy  in  .         .118 

auricular  wave  in    .         .  .         .118 

significance  of         .         .  .      117,238 

VENTRICULAR  LIVER  PULSE        .    124 


INDEX 


419 


VENTRICULAR  MUSCLE 
action  on  a. -v.  septum    . 
insertion  of     . 
relaxation  of 


PAGE 

16 

16 

80 


\^ENTRICULAR  OUTFLOW      .         .       80 

VENTRICULAR  PRESSURE-CURVE    108 

VENTRICULAR  RHYTHM 

definition  of             ...  xx,  175 

due  to  heart-block           .         .  .182 

inexcitability  of  the  ventricle  in  .     189 

starting-place  of     .         .         .  .     143 

symptoms  associated  with      .  .187 

VENTRICULAR  SYSTOLE 

action  of,  on  auricle  ...  16 
retraction  of  structures  due  to  .  81 
shock  due  to    .         .         .         .         86,88 

VENTRICULAR  VENOUS  PULSE 

different  forms  of    .         .         .         .116 

VENTRICULAR  WAVE 

in  a  jugular  pulse    ....     110 

VERATRIN 

action  on  tonicity 

VERONAL 

VISCERA 

insensitiveness  of    . 


9 

251,270 


VISCERAL  DISEASES 

classification  of  symptoms  in  . 
diagram  showing  mechanism  of  re- 
flexes in      ....         . 
effect  of,  on  spinal  cord  . 


34 


33 

36 
37 


VISCERAL  DISEASES  {continuci)— 

hyperalgesia  in  ...  .  55 
mental  state  in  .  .  .  .55 
reaction    of,    on    central    nervous 

system 55 

VISCERAL  REFLEXES 

purpose  of 37 

VISCEROMOTOR  REFLEX 

in  angina  pectoris            ...  41 

in  cardio-sclerosis            ...  41 

in  old  age        .....  41 

VISCEROSENSORY  REFLEX          .  35 

in  angina  pectoris  ....  40 


WARMTH 

feeling  of,  in  exophthalmic  goitre  .     133 

WASTING 

in  heart  failure        ....     209 

WATER-HAMMER  PULSE        .         .     240 

WHISKY 

during  an  attack  of  angina  pectoris      .53 

WHORL 

muscle- fibres  constituting       .         .       16 


WORRY 

effect  of  on  heart 


X  DISEASE 

and  the  sinus  irregularity 
slow  pulse-rate  in   . 
symptoms  of  the     . 


.     270 


146 
139 

60 


^    Y?''  MAY   i  U  133D 


^T^-'-r^ 


